Science topic

Autoimmunity - Science topic

Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
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Anti-NDMAR encephalitis is a newly defined form of autoimmune encephalitis
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Is anyone interested for investigating the possible autoimmune implications in long-lasting Covid-19 symptoms? I am looking to have access to plasma or serum samples from patients who are experimenting post-Covid 19 symptoms more than 3 to 6 months after the disease. I can test for the presence of some autoantibodies in these specimen.
Should you be interested in a possible collaboratioon, please contact me through RG.
Thanks a lot.
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Are you looking at long COVID-19 infection or post COVID-19 symptoms and infections ?
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A 50-year-old woman with an autoantibody detected for 19 years has been showing increased tinnitus and mild hearing loss. Although recent literature is scarce in this approach, is anyone studying AIED and anti-cochlea? Thanks
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It has a definite relation
I can give you literature in abundance on this
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About our paper: First Case of Evidence of Rare Autoimmune Encephalitis in Patient with Severe Sars-Cov-2 Pneumonia and History of Chronic Alcoholism. Your Experience?????
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Thanks a lot!!!!!
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I came across some recent articles that suggest that the ratio of Th17 cells to T reg cells is important indicator of inflammation and autoimmunity. Would it make sense to use the markers CD3 (pan T cell marker) and CD25 (T reg cell marker) to determine cell population and conclude based on this the propensity for inflammation progression/autoimmunity?
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I think it is possible
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Despite exclusively killing us through an autoimmune reaction, why Covid19 is not classified as an autoimmune disease? Maybe because it is considered there is no vaccine solution for autoimmune diseases?
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COVID-19 is associated with hyperactive immune responses in both chronically ill and healthy individuals. While autoimmune diseases do experience altered immune system function, even though the ability to fight off pathogens is not necessarily weakened; rather the response is misguided.
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Is there a certain boundary between immune-modulating and autoimmune response in case of COVID-19? What is your opinion?
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Dear Vice-Rector of Research Dr. Normakhamatov!
You spotted a highly relevant point. Humans might slowly toward the future able to develop better immune - resistance with healthier lifestyles, but the more rampage COVID-19 becomes and the more dynamically it can spread out all over the globe the less likely this immune - resistance would develop due to new emerging mutations and climate change:
1) Wagner Gouvêa dos Santos (2021). Impact of virus genetic variability and host immunity for the success of COVID-19 vaccines, Biomedicine & Pharmacotherapy
Volume 136, April 2021, Citation: "Even if COVID-19 may be brought under control in the near future, unexpected outbreaks and development of SARS-CoV-2 resistant to treatments or even vaccines are highly possible due to new mutations."Open access:
2) Gorji, S., Gorji, A. COVID-19 pandemic: the possible influence of the long-term ignorance about climate change. Environ Sci Pollut Res (2021). https://doi.org/10.1007/s11356-020-12167-z Citation: "Multiple lines of evidence suggest that the large-scale and rapid environmental changes in the last few decades may be implicated in the emergence of COVID-19 pandemic by increasing the potential risk of the occurrence and the spread of zoonotic diseases, worsening food security, and weakening the human immune system. As we are facing progressive climatic change, a failure to act accordingly could inevitably lead to further, more frequent confrontations with newly emerging diseases.Open access:
Yours sincerely, Bulcsu Szekely
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I'm aiming to use an adoptive cell transfer approach, with microglia in mice with ALS. So far all the protocols I have seen, require sacrificing the mouse. I'd like to re-infuse the microglia back into the same original mouse, once I've over expressed a receptor using lentivirus transduction.
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no, it is not possible. microglia does not circulate outside the brain, so you need the brain to extract it. But: you can derive microglia from murine iPSC lines, modified with your virus, and then inject it into mice in which you have ablated most microglia using a CSF1R inhibitor. Cool experiment this would be....
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BACKGROUND. I am not a molecular biology expert. I am a retired rheumatologist who dealt with autoantibodies and autoimmune diseases. Rheumatology has been caught up in COVID-19 business via often misguided appropriation of its treatments (hydroxychloroquine, corticosteroids, biologics and colchicine), via patients being sometimes deprived of those treatments because back ordered (rheumatoid arthritis, systemic lupus erythematosus) and via COVID-19 syndromes mimicking rheumatic diseases (Kawasaki in children, anti-phospholipid/lupus/vasculitis and other autoimmune syndromes in adults)
RATIONALE. Currently there are two types of anti-COVID vaccines: the novel, viral-mRNA-driven approach and the classical, viral-protein-driven approach. In the mRNA scheme, delivery of functional mRNA to macrophages, its use to make viral spike protein and its rapid degradation are all within current theory. A marvellous technological achievemen!
QUESTIONS.. What is known about the intracellular processing and migration towards the cell surface of the auto-produced spike protein, about its membrane incorporation and about its presentation as an antigen? Is there any self-membrane moiety wether lipid or protein linked to the spike protein polypeptide? Is there any spike protein shedding and then, does it behave as a regular protein vaccine? While on the cell surface or while shedded, are there neoantigens created which would be part auto, part exo-antigen?
IN SHORT, is there any possibility or evidence of inducing downstream, weeks or months post mRNA vaccine, new auto-immun phenomena or diseases? Currently, there is little or no data to support my worries and, as far as I know, there are no plans to collect any long term follow-up data,. Should there be some?  Replacing the COVID-19 pandemic by a man made autoimmune disaster would be the ultimate victory of this most devious virus.
I welcome reassuring thoughts, scientific data, clinical observations or comments?
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Covid_19mRNA vaccine is novel one,so great care should be cosidered with autoimmune phenomena because vaccine may trigger the disease
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This is a external quality control material I am looking for my autoimmune lab.
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In India, RML Mehrotra Pathology Pvt. Ltd & Dr Lal Path Labs, I guess !!!
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Remdesivir has been shown to speed up recovery times for patients with COVID-19 in a major US-led trial, becoming the first drug with proven benefit against the disease. Now, considering the biphasic attitude of the disease which seems to act as a direct viral insult at the beginning and then like an autoimmune response similar to what is observed in Hemophagocytic lymphohistiocytosis, the anti-viral treatment should given before this might happen.
I wish to know the opnion of the scientific community on this hot topic.
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Hello Piergiorgio
I would wait to read the full work before making a final judgment. In fact, the data that have been disclosed do not seem exciting to me. The trial was correctly sized, yet the most important outcome - mortality - was not significant. It is necessary to understand whether the observed mean effect can be diversified, with a greater effect in patients with earlier disease compared with patients with advanced disease, even if all enrolled patients were in a quite advanced phase. Anyway, I believe that with remdesivir we are far from having “the cure” for the disease. After all, we need antivirals specifically designed for Sars-Cov-2. In fact, all the antivirals tested in this setting have a binding affinity for the virus that can never be optimal, since they are not specific for this virus. As a consequence their effect, if ever present, can only always be modest.
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SARS-CoV-2 mainly affects the elderly, predominant in rich countries. Developing countries can more easily overcome the pandemic, given their lower life expectancy and that young people are less affected. Autoimmunization may be faster, and demographic and economic effects could be reduced in the long term
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Rich countries have more resources to get a quick recovery in general....
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Specifically, does the cyclic drop off in estrogen trigger a change in immune function? What is the relationship between the estrogen peak and inflammation? Most papers I've looked at expose immune cells to a steady-state concentration. Do you know of any reports where immune cells were cultured at cyclic estrogen concentrations and harvested at different times to see the effect?
(This is far outside my field so please forgive if I'm asking a basic question that is common knowledge in the places where immunology meets reproductive endocrinology.)
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Thank you Suhad Mohammed for the link to that review. Only one paper the authors referenced (Ref. 44), said anything about the cyclic nature of immune function. That paper does not appear to be indexed in PubMed and only demonstrated that there are an increased number of white blood cells present in females during the proliferate phase. Do you know of any papers that speak directly to the activity of leukocytes (cytokine production, reactivity to LPS, etc.) over the menstrual cycle?
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I am struggling over the search for studies showing that the age of an individual has an impact on the increased prevalence of Rheumatoid diseases. Wouldn't that be rather a stochastic issue (the longer the time, the higher the chance)? While I could imagine, how increased incidences of cancer correlate with age or that infections result in increased mortality with age, I am struggling about how the cellular age results in autoimmune disorders. I read about thymic atrophy/less T cell variablity and changes in B cell responses and alterations in Tfh cell reactivity and alteration in phagocyte functions (less phagocytosis, less radical synthesis), but does that necessarily lead to an increased incidence of autoimmunity? And if autoimmunity is posively correlated with age, shouldn't the overall response during a particular period be stronger in old organisms than the same disease of comparable period in younger organisms?
UPDATE (March2020): I would say that depending on the autoimmune disease, age shows a positive or negative correlation. However, I am still looking for publications with valid in vivo models showing the age effect on the disease outcome or not.
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That is interesting regarding the poor Treg function in RAG1ko‘s. Sorry that the paper was of no help to you, as I said it was a quick google search but is obviously 2013! Would you be able to let me know what you find out?
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Recently cytomegalovirus is shown to infect human pancreas islets. I wonder this virus will modify IA-2 antigens in these tissues.
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Have a look at this useful RG link.
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Pemphigus vulgaris is an autoimmune bullous disease. It is one of the difficult to treat conditions. Some cases of Pemphigus vulgaris are difficult to control even with high doses of systemic corticosteroids, other immunosuppressive agents and biologics. As diets containing thiols, thiocyanates, phenols and tannins can precipitate pemphigus in a genetically predisposed individual, it is logical to think that dietary restriction may help in disease control. Then what could the dietary advice to a patient with pemphigus vulgaris?
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High consumption of foods containing tannins, thiols, phenols, misothiocyanates and phycocyanin should be avoided. A list of foods containing these substances includes garlic, leek, chives, onion, mustard (thiols), black pepper, red chilies, mango, pistachio, cashews, aspartame, food additives (phenols), mango, cassava, yucca, guarana, betel nuts, raspberry, cranberry, blackberry, avocado, peach, ginger, ginseng, tea, red wine, coffee, spices, eggplant (tannins), mustard, horseradish, cauliflower (isothiocyanates) and Spirulina platensis alga (phycocyanins).
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Neopterin is a bio-marker of cellular immune activation, its associated with viral, intracellular bacterial, autoimmune, and certain cancers. It can be quantified by blood serum analysis (Lab or POCT) or by shipping urine off to a lab. Is there a POCT that anyone recommends for quantifying it in the field? If not, Is there a similar bio-marker that can be used instead?
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Neopterin is not assessed commonly in POTCs. You can quantify it only in cental labs or research labs
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Fetal microchimerism is established during pregnancy and abortion. This has been linked with development of autoimmunity in females. Various hypothesis have been proposed for how microchimerism is associated with autoimmune diseases but no consensus has been formed.
What are the techniques to identify fetal microchimerism in autoimmune diseases in females?
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I have heard at a conference, but missed the reference, that evidence suggest latent TB could protect against re-infection. Does anyone have heard about that, and have references in mind? (The dogma says the opposite, that latent TB does not protect against re-infection).
Cheers!
Olivier
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Please go through the following RG link.
Thanks!
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In Dermatology practice every now and then we deal with diseases where there is a need of long continued oral corticosteroid prescription. In some cases like autoimmune bullous diseases high dose corticosteroids are usually prescribed. When there is a control of acute episode there is a need of tapering the doses though in many cases it is impossible to withdraw the corticosteroids. Usually, I follow the rule of 20% dose decrement at an interval of 2 weeks or when there are signs of disease improvement. Do you think, what is followed by me is ideal? or Is there any better and easier option for tapering?
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I think immediate cesation of steroids is possible in cases of less than 2 to 3 weeks of therapy.
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Just wanting to find out if it is possible to to use T cell therapy as a treatment for Haemolytic disease of newborn as T cell therapy is used in autoimmune treatment.
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Dear it may not be the best treatment because you have to look at the cause of the HDN is it ABO incompatibility or Rhesus blood group associated HDN which you will solve in that direction.
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Please help. I am doing a systematic review of largely observational studies on the safety and effectiveness of treating autoimmune alopecia with Hydroxychloroquine in older adults. I was wondering if a subgroup analysis is feasible in a SR based largely on observational studies. Thank you.
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Subgroup analysis is feasible, provided that analysis according to the factors that you want to subgroup is provided in included or some of the included papers. Otherwise you should opt for individual patient data analysis. Rather than subrgrouping you can also consider meta-regression analysis taking in mind the factors that you want to adjust for. This might be more feasible in certain cases.
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Please help. Understanding immune privilege is largely viewed as integral to unlocking optimal treatment options for autoimmune sufferers. Yet there is a clear sexual dimorphism in autoimmune disease. Is there any correlation between immune privilege and gender?
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This is a fascinating question. Immune privilege can be thought of as antigens hidden away from the immune system by either physical (i.e. blood-brain barrier) or immunological barriers. Immunological barriers include low expression of MHC proteins, high balance between regulatory and effector cells or expression of protective molecules such as Fas or immune suppressive cytokines such as TGF-beta (as suggested as mechanisms of immune privilege in the anterior chamber of the eye). The reason that females are more susceptible to males for most classical autoimmune diseases, with exceptions being type 1 diabetes, myasthenia gravis, pemphigus vulgaris and Goodpasture's syndrome, is not clear. Some authors have suggested that women make stronger inflammatory responses to infectious agents than men because their survival is more important for continuance of the species. However, the detailed mechanism of this is not clear.
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I am looking for a step-by-step protocol for detection of anti-granulocyte Ab (diagnosis of autoimmune neutropenia). Thanks.
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in addition to the very valuable papers from Thomas, take into account of you wanna use the recombinant HNAs or extracted HNAs or the whole cells.
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I am currently looking for some papers on Biological therapies (preferably animal studies) on the use of monoclonal antibodies to attenuate Experimental Autoimmune Encepelomyelitis, Or the application of Treg cell therapy to ameliorate autoimmune disease. Any help would be greatly appreciated.
Best wishes,
Carl.
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Hello,
Have you tried with Google Scholar? You usually have different websites referenced for one paper, and on some you have access to the full article.
You can also contact the corresponding author (or the first) and ask for the full text.
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PBC is a chronic liver condition resulting from progressive destruction of the intrahepatic bile duct and eventually leading to cirrhosis.
Knowing that PBC might have an autoimmune etiology, why isn't it treated with immunosuppressive therapy (like: corticosteroids, azathioprine.. etc)?
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I think the pathogenesis of PBC is not understood well enough at this point. See for a nice review of the subject. Some immunosuppressives that have been evaluate in PBC were somewhat beneficial but usually at the cost of high toxicity.
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Chronic autoimmune skin disease. This condition occurs when the immune system sends out wrong signals .These signals increase the speed of the skin's growth cycle, that is, excessive increase in skin cells from the amount of shedding them.so I want to know that can we prevent this wrong signals by using things like electrodes.?
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Still needs more trials though. But I think it's a good start to find molecular evidence behind this;)
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Subjective experience in a hot near-desert climate with extremes of hot and cold temperatures during the year
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It seems Yakubu Lawal doesn't care. When researchers answer here, it's after considerable effort.
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I am actively engaged in the research work pertaining to phytochemicals and finding out the mechanism of their action. The diseases in consideration are autoimmune and inflammatory in nature. I hope to contribute significantly in this project. Please send the required formalities to fulfill.
Thanks and Regards
Debasis Sahu, PhD
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agree with @ M. Jameel
regards
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We have a research problem. We have various patients with a very unknown rare multisystem disease, of presumed autoimmune origin (since it can be managed with immunosuppressive agents.)
We would like to identify the type(s) of antibodies responsible for the disease. We have tried the standard and not so standard panels without results. A couple of patients showed some indeterminate neuropilar labeling on some macaque brain slides.
Anybody knows a way to identify antibodies in plasma/ serum adequate for this case?
We are happy (and eager) to collaborate.
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I would make SDS/reducing lysates of whatever tissue you think is the target of these antibodies, and analyze by Western blot with patient's serum. Comparing more than one patient's serum as well as normal controls will help you identify specific targets. Remember that human sera will bind a lot of proteins, so be sure to titer it down. After you have identified a protein of specific mass, you can cut it out and do mass spec for identification.
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I would like to know what subtle differences exist between cancer(altered self) cells and autoimmune cells; esp. in their level of expression of specific markers.
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Thank you all for your answers. However, my curiosity is also in line with Geraldo's question. Cancer cells thrive in an immune microenvironment bypassing the body's natural self-defence. A number of pathways have been validated as well in lieu of cancer-immunity crosstalk. Are there reported interactions among transformed cells and immune cells which may alter the morphology of immune cells, keeping in view structural alterations of participating proteins presented on the surface of either category of cells?
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Is there anyone who has information in regards to ELISA analysis done on crocodilians? Looking to assess parasite load and immune response in crocs, but I can only find one article who's tried this semi-successfully.
Is there a other/better way to measure immune response, or the lack of, in crocodiles in response to parasite load?
Cheers
Joe
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Hi Dr. Al-Salhie, unfortunately your link shows an equipment that is called "Crocodile" ( the commercial name of the instrument is crocodile, a device to pipette, wash and incubate plates only). However, Berthold technologies does not sell ELISA assays directed to crocodilian proteins, just as nobody else does for reptiles. Believe me, I searched everywhere for antibodies against snake proteins.
Thank you though, for a split second my hopes were high...
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It has been reported recently that industrial dairies favor super-productive cow breeds (Holsteins, mostly) that give milk with a protein known as AI which has been linked to serious health conditions (e.g., diabetes, heart disease, and autoimmune conditions like eczema and asthma).
Does anyone have more detailed information?
Does milk from all sources contain AI protein?
Does milk produced by grass-fed cows from organic dairies contain AI protein (or just less)?
Does breast milk contain any AI protein?
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A single amino acid in the milk protein beta-casein makes the difference between A1 and A2. The A2 casein at position 67 contains the amino acid proline, and the A1 casein histidine. Thus, in the digestion of A1, the so-called opiate beta casomorphin-7 (BCM-7) is split off, not in the A2 varinates. This metabolite is said to be the reason that some people can not tolerate milk.
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Antibody-testing in Susac syndrome - antigen target and availability of analyses.
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Susac syndrome is one of the differentials we MS specialists keep in mind when we diagnose multiple sclerosis. to date i am not aware of any serologic or CSF test for this disease. it is based on history, physical and MRI which shows the distribution of white matter lesions that is very similar to multiple sclerosis except for some slight differences which can be missed by the untrained eye. thanks.
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I am noticing though subjective, a substantial number of autoimmune conditions in a Northeastern Nigerian location, hot quasi desert climate
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Probable there is a reverse relationship between the climate and the onset of autoimmune diseases. They predominate in humid and cold climates generally speaking
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Stress Autoimmunity Thyroid disease
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Yes. both your answers were very helpful. Just what i was looking for.
Tank you very much.
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It is my understanding that Tregs can influence development of autoimmunity through complex signaling pathways. Since they are often at high levels in progression of breast, ovarian and pancreatic cancers, I was wondering whether this is due to what's going on inside these tumors or their environment as a chemical process that may increase Treg production or differentiation, or whether the high levels of Tregs result from a patient's depleted immune system?
Can strategies be targeted selectively on reducing Tregs if they are interfering with a patient's response to therapy?
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Different strategies including the use of depleting/blocking antibodies (CD25, CTLA-4, CCL2), IL-2/immunotoxin conjugates, cyclophosphamide, or COX2 inhibitors have been tested in mouse models of cancer and pre-clinical trials, but these did not always result in decreased numbers of Tregs or good anti-tumour response (see: Beyer & Schultze. 2006. Blood 108(3)804-11. https://www.ncbi.nlm.nih.gov/pubmed/16861339).
Frederick Arce, in Sergio Quezada’s group (University College London Cancer Institute), has recently published a paper in which they report on the importance of the anti-CD25-depleting antibody isotype in mouse models of transplantable tumour cell lines. They found that using engineered anti-CD25 antibodies with increased binding to Fc receptors results in enhanced depletion of intra-tumoral Tregs. This antibody, used in combination with immune check-point therapy led to complete tumour rejection in mice. Their observation that CD25 expression is restricted to CD4+Foxp3+ in human peripheral and tumour-infiltrating lymphocytes led them to propose that this validates the use of CD25 as a target for therapeutic Treg depletion in humans.
Very interesting paper (https://www.ncbi.nlm.nih.gov/pubmed/28410988) to read and see where the field of combined immunotherapy for cancer is moving. Their results suggest that efficient depletion of Tregs would be possible in clinical trials in order to improve the response to other therapies.
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The porosity of the liver fenestrated sinusoidal endothelial cells is all important in atherogenesis & lipoprotein metabolism. LSEC porosity balances dietary cholesterol with that synthesised by the liver, being transported in lipoproteins of different sizes (chylomicon remnants , VLDL, LDL & HDL cholesterol). Many other metabolic diseases such as diabetes, hepatic steatosis and fibrosis may also relate to LSEC fenestrations and porosity.
Simple tests are necessary to correlate cause and effect in the epidemiology and treatment of these porosity related diseases.
I applaud this exciting advance since it should confirm a role of LSEC porosity with multiple diseases, such as those related to autoimmunity.
For multiple clinical diagnoses , protein bound dyes such as ICG, BSP or other simple Liver Function Tests are required for hospital or epidemiolical scrutiny. This present description of super-resolution by optical microscopy hopefully may further confirm these dye tests as a true measure of LSEC porosity.
I am excited by this research method and predict fascinating future findings.
Robin Fraser, Pathology, University of Otago, Christchurch, NZ.
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You "applaud" to your paper?
Interesting.
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Is there a comprehensive (perhaps proteomics-based) approach that will screen out autoantibodies from blood and also (reliably) predict their target? I am interested in autoantibodies against CNS antigens. Any other simpler method not involving omics is also welcome.
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Hello,
I'm looking for a method to evaluate autoimmunity (disease-severity score) in B6/AIRE KO mice.
I was advised to use immunohistochemistry of the eye, liver and salivary glands. However, I would like to have more quantitative method as ELISA (preferably not with a kit).
Any help/ suggestions will be highly appreciated!
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Thanks a lot, Michael !
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I have read it somewhere in an article that avian defensin mRNAs have been found abundantly in the bone marrow and their proteins in heterophil granules, so I was wondering if someone is working with avian blood samples is there any possibility of getting defensin's RNA from blood?
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I am using Trizol reagent for RNA isolation and i have isolated RNA easily there was no such issue of erythrocytes or thrombocytes. The thing I am worried about is that most of the defensin's transcripts have been isolated from other tissues not blood now I just hope to get altleast some of the transcripts from blood as well.
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In systemic erythematosus lupus (SLE) anti-dsDNA antibodies can be detected. When we talk about antibodies we usually think about proteins that bind proteins. However, there are also antibodies that bind other molecules such as DNA. Can you point to some research that explains this process in detail. It is somehow not intuitively clear to me how and why would an organism do it. Also, would the specificity of such antibodies be valid? Is process of anti-DNA antibodies physiological of strictly pathological?
I would be grateful for your comments.
Best,
Jan
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There is some older literature supporting and pushing the idea that anti-DNA antibodies are actually anti-protein antibodies that cross-react with DNA, but there is no fundamental reason to adopt this notion.  As Jing Zhang pointed out, antibodies can potentially react with just about any chemical/biochemical molecular target, based purely on serendipitous affinity of non-covalent chemical bonds between the antigen and “complementarity-determining regions” of the antibody.  (In some cases monoclonal antibodies can even react with disparate antigens not because of true cross-reactivity but probably due to alternative or overlapping binding sites within the CDR.) Nevertheless, the process for production of anti-DNA antibodies in SLE is likely the same as that for induction of any antibodies – the presence in the human of a B cell that happens to have BCRs with an above-threshold affinity for native DNA and which receives “help” for its activation and affinity maturation by T cells. The existence of such B cells is explainable by the huge B cell repertoire and the inefficiency of B cell tolerance mechanisms.   The pathological event, in my opinion, requires the co-presence of autoreactive T cells that had not been tolerized to a peptide ligand derived from a protein that is physically associated with DNA.  Histone-reactive T cells would be obvious candidates, and such T cells could also provide help for autoreactive B cells with receptors for histones or for histone-DNA complexes (nucleosomes/chromatin), which are also common in SLE.  In addition naïve autoreactive T cells would probably also require pre-activation by “professional antigen-presenting cells” presenting the same ligand, but how this happens is more of a mystery. You ask why would this happen: the only (unsatisfying) answer is that the immune system is inherently flawed or imperfect.  Autoimmunity is a side-effect of the evolutionary drive to create an immune system that can anticipate and respond to just about any pathogen.
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Conflicting data appears to exist as to whether vitamin D induces apoptosis. Do you have any evidence as to whether is does or does not?
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In breast cancer cells, calcitriol has an antiproliferative effect, but it does not induce apoptosis. Nevertheless calcitriol enhances the apoptotic effect of other antitumoral drugs. You can review the following article Journal of Steroid Biochemistry & Molecular Biology 148 (2015) 122–131
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type 1.5 diabetes is the late onset of autoimmune type 1 diabetes
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Type 1.5 diabetes is a non-official term that is sometimes used to refer to a form of type 1 diabetes known as Latent Autoimmune Diabetes in Adults (LADA). The term type 1.5 refers to the fact that the condition is a form of type 1 diabetes that can share some features that are more commonly associated with type 2 diabetes.
Type 1.5 diabetes is sometimes also called as type 3 diabetes or “double diabetes,” because the adult has aspects of both Type 1 and Type 2 diabetes. Type 1.5 diabetics are said to have “double” diabetes because they show both the autoimmune destruction of beta cells of Type 1 diabetes and the insulin resistance characteristic of Type 2 diabetes. People with Type 1.5 have autoantibodies and gradually lose their insulin-producing capability, requiring insulin within 5–10 years of diagnosis. As their insulin resistance suggests, many people with Type 1.5 diabetes are obese or overweight.
Misdiagnosis as having type 2 diabetes is common. Around 15-20% of people diagnosed with type 2 diabetes may actually have Type 1.5 diabetes.
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As has been suggested and proven, among multiple triggers of autoimmunity, some infectious diseases agents, would do that. My question, which are the most likely viruses that can induce autoimmunity?
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Autoimmune reactions often result from infection with a virus. The HLA system cuts pieces (8-10 a.a. for Class I to CD8+, longer for Class II to CD4+ T cells), of viral peptides. This helps in recognition and destruction of infected cells, but if the HLA type captures the same fragment of a normal protein like MBP, this results in auto-immunity. So, the only requirement is for a systemic infection, but viruses which target long-lived structural cells will often trigger more auto-immune reactions than those infecting epithelial or blood cells. So, its more of an HLA and self-T cell repertoire. 
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What is the difference between collagenase D and collagenase II? Does anyone know the optimal collagenase for digestion of human cartilage?
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Collagenase D prepared from Clos. histolyticum ihas high collagenase activityand very low tryptic activity. Collagenase 2 has a highLipolytic activity from fat cells
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If mRNA would get into the endosomes of human cells would it be recognized by TLR7/8? And if it would be recognized, would it be immunostimulatory, or does the 5' cap and 3' poly A-tail prevent that reactions toward self RNA occur?
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I have tried transfection of cellular RNA into 293T cells by lipofectamine, the cellular RNA did not stimulate the cells to produce IFN. the transfection of RNA by lipofectamine may directly deliver the RNA into cytoplasm that avoid to be recognized by TLRs. 
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I am planning to isolate and analyse the nucleosomes and methylation status of the circulating DNA from the autoimmune mice models. There is a lot of information available for human blood but not much for the same in mice. How much serum/plasma from mouse is enough? Any information would be helpful. Reference to any available literature would also help. 
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Dear Monica,
I usually take 200 µl of mouse blood for standard genotyping. How much DNA do you need for your analysis?
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a possible cause of autoimmunity from exposure in a high moisture water damaged building? I'm thinking very possible and found a couple articles of interest, any out there specificly about this?
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if one of the causes or the causes of ME/CFS is chemical exposure, than how autoimmunity may accure leaves the possibility of molecular mimicry open if there is any truth to it, or weither it depends strictly on immune malfunction, loss of homeostasis, than what would fallow would be seceptability to infection, just because viruses are often found does not mean they are the cause.  I know for a fact that severe exposure in a high moisture water damaged building can lead to ME/CFS, I know that I'm highly sensitive to certain chemicals and voc's along with allergens. if molecular mimicry can happen this type of exposure would be a very likely contender, just keeping a open mind and asking questions, but ya, I would think you could see my interest in the subject, I understand your view.
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For the case of any autoimmune disease there does not exist any disease free equilibrium point as well as any Basic reproduction ratio(R0). So how we can introduce impulsive drug therapy to control the disease.
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Dear Amit~Chronic Disease is an intracellular infection: www.mpkb.org
Benicar(olmesartan) 40 mg every 4-6 hours, acting as a VDR agonist, will partner with the innate immune system to reverse the autoimmune condition.  The drug therapy can be introduced clinically to patients who are motivated to follow the Marshall Protocol and able to tolerate the immunopathology that results from pathogen die-off.
See www.np-privatepracticeassoc.com for some case study series results over 4 years.
Then register for www.MarshallProtocol.com to check out the worldwide cohort utilizing this method.
Our newest paper:  https://t.co/FY4xMjzFF9 
A prior paper: bit.ly/2af83oU
Please let me know if I can be of further assistance.
Sincerely,
Trudy J. Rumann Heil MS, ARNP, CLNC
Scottsdale, AZ USA
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I want to work on mouse Erap1 gene. I design the primer but its not specific and I couldn't find any reference for the mouse Erap1 primer. Can any one help me out please!!!!
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Hi
look PDF attached and these links PLZ
ERAP1 endoplasmic reticulum aminopeptidase 1 [Homo sapiens ...
www.ncbi.nlm.nih.gov/gene?Db...National Center for Biotechnology Information
Jul 3, 2016 - epistatic interaction between ERAP1 and the HLA class I alleles .... have orthologs with human gene ERAP1; Map Viewer (Mouse, Rat) ...
Erap1 MGI Mouse Gene Detail - MGI:1933403 - endoplasmic ...
Mouse Genome Informatics
View mouse Erap1 Chr13:74639872-74691875 with: phenotypes, sequences, polymorphisms, proteins, references, function, ... Erap1. Name. endoplasmic reticulum aminopeptidase 1. Synonyms. Arts1, ERAAP, PILSAP .... Primer pair 1.
QIAGEN - Products for Erap1 (Mouse)
Qiagen
GeneGlobe Products for Erap1 (Mouse) Full Name: endoplasmic reticulum ... EpiTect Methyl II PCR Primer Assay for Mouse Erap1 (CpG Island 103126).
The Role of Endoplasmic Reticulum-Associated Aminopeptidase 1 in ...
Journal of Immunology
by E Firat - ‎2007 - ‎Cited by 87 - ‎Related articles
We generated ERAP1-deficient mice and analyzed cytotoxic responses upon infection .... the Expand long template PCR system (Roche) with the forward primer.
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For exmple, in the study about autoimmune, how can we assess that there are any antibody bind to cell surface as start up 0f the graft rejection process.
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You could use the Coombe's technique (like the test used to diagnose autoimmune haemolytic anaemia)- wash the cells in PBS three times and incubate them with anti human immunoglobulin (antibody against human immunoglobulin which you can buy) and examine for cell clumping. If the cells have antibody on their surface, they will bind to the AHG and clump together. You can visualise the clumps under microscope. This is an easy test to do. Good luck 
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many patients are being tested for antithyroid antibody to rule out autoimmune cause. I frequently come around such patients .so is there any significant triggering factor for formation of these antibodies ?
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Many toxic chemicals have been linked to development of autoimmune thyroid disease (and it is prevalent in women with endometriosis).  The list of chemicals is very long --I'm sure you'll find them in the work of Thomas Zoeller.
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Recent findings show that ustekinumab may be a possible solution for many primary non responding psoriatic arthritis patients who failed all tnf blockers treatments (not patients who were forced to suspend the treatment because of negative side effects). Nevertheless there're still people who do not respond to ustekinumab even at 90 mg dosage.
Can anybody tell me the reason of this failure?
Can this failure be due to a "genetic settings" of patients' autoimmune system which can defeat monoclonal antibodies which are used both with ustekinumab as with tnf alpha blockers?
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Grazie mille Angelo. Speriamo in questo Jak-treatment di cui mi parlavi proprio tu tempo fa.
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I am looking for the effects of trust versus mistrust that could lead to significant trauma psychologically, and eventually lead to breakdown of adrenal gland or autoimmune functioning and lead to disease or new medical symptoms.
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Kind regards for the articles you forwarded. I will take a look at them this week.
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Do someone have informations / references about Myelodysplastic-like morphologic changes in trephine bone marrow biopsy, NOT due to chemotherapy or viral diseases, but associated to lymphomas or non hematologic diseases like autoimmune or chronic inflammatory processes. A PubMed search did not give useful results.
Thanks a lot for any help. Philippe 
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Dear colleague,
I personally have seen changes in bone marrow morphology in lymphoma patients prior to any chemo. Mostly, I saw changes in eritroblasts such as binuclear cell morphology, or mitotic figures. Sometimes I saw micromegakaryocytes or pseudo-Gaucher cells. This is rare events. The origin of this changes is unknown to me. My own speculations may be that malignant cells and their microenvironment may produce some cytokines, or substances that disturb regular hematopoiesis. Of course, this need to be evaluated through serious investigations. 
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Human Endogenous Retroviruses (HERVs) can participate in numerous diseases, especially autoimmune, (neuro)degenerative, cancers, etc. 
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ERVs have been around for a very long time and have altered immune responses in many species including in humans (see the link). Depending upon the type of ERVs, their numbers in the human genome, and the regulatory sequence they harbor, it is likely that these ERVs in humans contribute to the number of outcomes, including those you mentioned.
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Is rituximab useful in patients with myastenia gravis with and without rheumatic inflammatory diseases or HCV infection ?
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Biribidobiribbu'  
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  1. How long would you expect auto-antibodies to be present in CSF in autoimmune encephalitis?
  2. Would there be any difference between untreated and treated (IVIG/rituximab) cases?
  3. Could you perform a lumbar puncture several years later in untreated patients and still be able to detect the auto-antibody (AMPAR 1/2, NMDAR, GABA-bR, VGCC, CASPR-2, VGKC)?
Thank you for your time and help!
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Several aspects have to be kept in mind when discussing the persistence of auto-antibodies in the CSF. In the case of paraneoplastic syndromes the source of autoantibodies are presumably plasma cells in secondary or tertiary lymphoid structures outside the CNS. Therefore, levels of antibodies in the CSF should be linked to serum levels. It has to be noted that paraneoplastic antibodies can persist for years, even when the tumor has been removed (Alexopoulos H  et al. Paraneoplastic anti-NMDAR encephalitis: long term follow-up reveals persistent serum antibodies. J Neurol. 2011 Aug;258(8):1568-70).
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Since undigested gliadin is the mechanism of the autoimmune reaction in Celiac Disease, I was wondering if anyone was investigating the degradation of gliadin and would appreciate any discussion on the topic.
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Dear Anthony,
With all due respect, while it is true that researchers and clinicians choose to measure the TTg antibody response as a convenience, and claim that this is a valid autoimmune response (rather than a result of a collateral reaction associated with a primary reaction against an exogenous antigen), this in no way proves or even infers that the primary inflammatory reaction is not directed at the gliadin and glutelin peptides resulting from the digestion of the gluten found in wheat and related species.
To support that observation I submit the fact that when the exogenous antigen is withdrawn from the diet, the TTg reaction ceases.  Obviously it is not an independent reaction.  So how could the TTg antibody response actually be a valid autoimmune response?  The answer is, "It cannot be a true AI response".  If the reaction were truly autoimmune, then it would continue, independent of the status (presence or absence) of any exogenous antigens in the diet.
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Autoimmunity reflects a biophysical response of a system reserved to own cells and tissues.  It could be also said that autoimmunity complements an evolutionary control / need of self-identification.
In 400 BC Hippocrates invented the word “apoptosis” in the book of Mochlicon—Hippocrates’ treatise on the reduction of dislocation- to describe the resulting gangrene - see: Esposti, "Apoptosis: who was first?" Cell Death and Differentiation, 1998; André 2003 "Hippocrates of Cos and apoptosis"- Lancet 361/1306; Mackay&Rose "The autoimmune diseases"  2013.  
Apoptosis and necrosis are fundamentals in control of human physiology and diseases. In another conception, autoimmunity results from the inhibition / inability / failure to control the Immune Response via cell death (apoptosis). 
Considering that biomedical sciences progress and merge to a System conception where the numbers should be behind the molecules, do you think that autoimmunity is just the other face (antipodal point) of an unsuccessful cell death / rejection control and in that sense autoimmune elements might have common properties despite distinct origins?
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Dear Jonathan,
I appreciate your analysis and your clarification.  I agree, it could be misleading to generalize in science. It is also important to accept that biomedical sciences are in search of concrete models that would allow to clarify the cause-and-effect of an observation.  Let’s take the hypothesis that we have to represent at one point of a circle autoimmunity. What would be the antipodal point?  Autoimmunity is cause-and-effect sequence and should exist a model to describe it by establishing: a) a concrete and safe cure for the case of diseases and b) a logic conception so to understand this cause-and-effect phenomenon.  
I think you agree that either in B or T cells, autoimmunity engages a selection system. You nicely said that B cell regulation is based on random diversification and selection rather than instruction.  I could say that instruction is also a selection system.
“Roitt and Doniach at University College London and others have shown that in terms of antibody-producing B lymphocytes, diseases such as rheumatoid arthritis and thyrotoxicosis are associated with loss of immunological tolerance which is the ability of an individual to ignore "self", while reacting to "non-self". “This breakage leads to the immune system's mounting an effective and specific immune response against self-determinants”.  This breakage might lead to autoimmunity.
*the term “self” and “non-self” is confusing as what could be considered as “non-self” at dt by the N-individual – the human genome is expressed to environmental stress including viral DNA, vaccination, bacterial threat etc - can turn to be “self” in dt+n and then recognized by the N+1 individual in dt+n+1 under a different environmental/genetic background as “non-self” and this might be an evolutionary perspective of autoimmune reaction leading to loss or instruction of immunological tolerance.  This can be addressed also in the light of viral infection and control of autoimmune levels and etc. The N-individual is part of a sequence of events including N+1, N+2, N+n individuals.
In the clonal deletion theory, proposed by Burnet and Medawar, self-reactive lymphoid cells are destroyed during the development of the immune system in an individual (Nobel Price 1960 acquired immunological tolerance).
So, both Roit and Burnet and others introduced in their approach of studding autoimmunity the term of “loss or destroy”.  Even if autoimmunity is driven by an ‘instructive pathway”; at the bottom line a healthy immune system has the capacity to make a decision using its “proper internal control” and decides to keep the self-intact and attack the non-self.  . If, autoimmunity engages a false elimination or destruction or an “instructive process” of a target (cell - molecule) which is involved in the autoimmune response then we have to ask what the machinery for this process is.
I could say this includes proteolytic machinery, proteasomes, ubiquitination, apoptotic machinery.  This should be the antipodal point of autoimmunity in the circle and this is illustrated best by the term apoptosis.
Last but not least, talking about AIRE, it should not be a special case and I would not considered it as a monogenic disease, as it is in general claimed. AIRE defines a spatial nuclear domain with concrete properties. So any reference to AIRE makes reference to nuclear space. In the same category, we could add PML, SP100 in PBC and more. Vassilis
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We are looking at DAMP in its role as mediator of inflammatory cytokines in muscle tissue. What is your preferred method for determining DAMP level?
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I hope that following information will be helpful.
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I would like to study the types of regulatory T cells , their efficacy ,recruiting capabilities and other features associated with treatment of organ specific autoimmune diseases.I didn't find the markers of those types of cells .
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Hi Omer, 
The IC marker HELIOS would be the most conventional way to identify nTreg and this has recently been shown to enhanced by the addition of Nrp1. This has been reviewed by Lin et al. 
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We developed an ELISA array for the detection of autoimmune liver disease related antibodies in our experiment. the identified results from ELISA array for M2, SP100, GP210, RO-52 positive sera are agreement with the results from EUROIMMUN KITS, but  the results for LC-1 are obviously different. Many "positive" sera identified by ELISA array could not be identified by EUROIMMUN KITS. Beside a possible cause of different antigen used, any other possibility?
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Keep in mind autoimmune liver diseases may have high titers of anti-albumin IgG. A sensitve assay can detect them, Is your solid matrix coated with hu or Bovine albumin/
is your buffer contain albumin? Check all and revalidate.
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We believe their may be extrusion of mitochondria out of the cell and that their s an autoimmune response to these extrusions. Is their an assay or test we could use to look at that autoimmunity?
Thanks
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One idea is to isolate sera from  your mice and see if they have antibodies to mitochondria.  I would recommend the Kallestad Hep-2 kit from Biorad.  This is designed to test for anti-nuclear antibodies, but the manual describes other autoantibodies you might observe including those to organelles.  Anti-nuclear antibodies might also arise as a secondary effect in your mice. Just substitute a fluorescent anti-mouse Ig secondary antibody for the one in the kit.  The only caution is that you may need a large cohort of both experimental and control mice (probably at least 20 of each) for statistical significance because autoantibodies do show up in control mice.
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Why hydroxychloroquine can treat primary ITP with positive ANA antibody and can't if it is negative? and what is the evidence?
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 Dear Ghada Abdallah,
There are 2 components to your question. Let me tackle the easy part first. 
1. Evidence for efficacy for Hydroxychloroquin in ANA positive ITP: It was always known that almost 5% of SLE might start with isolated thrombocytopenia alone. Mechanisms of immune thrombocytopenia in SLE differs from those observed in primary ITP and is probably multifactorial, including antiplatelet glycoprotein antibodies such as in ITP but also immune complexes, antiphospholipid antibodies, autoantibodies to the c-MpL receptor and megakaryocytes.
Since Hydroxychloroquin works so well in treatment of multiple domains in SLE, it was but natural to study it in SLE associated throbocytopenia too where it was found useful. Next, about 20% of all ITP patients are ANA positive without meeting the criteria of SLE and this was the natural target to be studied for the effect of hydroxychloroquin. Interestingly, ANA positivity in ITP has been shown to a risk factor of chronic ITP and resistance to classical second-line treatment for ITP.
In the 2014 study by Khellaf et al, they looked at both SLE with thrombocytopenia and ANA positive ITP who had failed multiple drugs and tried hydroxychloroquin on them. As expected the SLE group indeed did very well with 83% response but even the other group showed a robust 50% response. Considering the excellent safety profile of hydroxychloroquin, these numbers are very encouraging. If these findings are replicated, hydroxychloroquin will very likely make its way into ITP treatment guidelines soon.
2. Why does it not work in ANA negative ITP? 
Where is the evidence that hydroxychlororquin "does not" act in ANA negative ITP as stated by you. Evidence is just emerging that it might be useful to some extent in the ANA positive variety. It requires another study to prove its inefficacy" in ANA negative ITP.
It was a natural step to use a time tested drug like hydroxychloroquin with proven efficacy in SLE to the subgroup of ANA positive ITP (who do not fulfil criteria for SLE). The next logical step seems to be to compare role of hydroxychloroquin in ANA positive Vs ANA negative ITP. I am not aware of any study that has specifically looked at this aspect. Maybe you can plan one such study.
If we are able to show in future that hydroxychloroquin "DOES NOT" act in ANA negative ITP, then we need new studies to study molecular mechanisms to understand the "why". 
hope this helps
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I am trying to generate BDC2.5 cell line from NOD mice. Using as a principal source the work of Haskins & al 1988. However I am not very familiar with this kind of procedure. In their paper: they used 10^5 islet cells, 2x10^7 irradiated splenocytes as APC and 25% EL-4 supernatant as source of IL-2. The line was perpetuated by restimulating with islet Ag, APC and IL-2 every 2 week, with a maximum 10^6 responding T cell used to seed the culture.
- Do I absolutely need IL-2, since I have read that it was not necessary for the generation of autoreactive T cell?
- What do they mean by "perpertuating the line": they keep adding new cells every 2 weeks without discarding the dead cells?
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Mo,
A better and easier alternative for you will be to contact the authors of publication and request them to provide the cells you intend to use.  With a material transfer agreement, most scientists and institutions are willing to share such resources.
If you must create your own cell line, you will have to use identical conditions as described in the original work. And even then, the cells line you isolate and propagate, may or may not be nearly the same, much less identical - another reason to acquire the same strain.
Best...
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There is no explanation between these two genes in literature. I need some words explaining the assessment of them in autoimmune and inflammatory diseases regarding my future research.
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PARP-1 is involved in to regulate the pathogenesis of inflammation. PARP-1 also plays important roles in other disease processes, like central nervous system dysfunctions (e.g. Stroke, Parkinson), carcinogenesis and autoimmune diseases such as type I diabetes. Tregs is important for in autoimmune and inflammatory diseases.PARP-1 can affect regulatory T cell differentiation. Tregs regulate immune responses by cell-cell contact via CTLA-4.  
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According to previous research, arteriole remodeling through inflammatory vasculopathy is attributed to PAH due to SLE.  Do any of you have any experience treating this condition through immunosuppression like cyclophosphamide, DMARDs, or even paradoxically corticosteroids?  Are there any other pathophysiological mechanisms linking inflammatory conditions to PAH?  Thank you.
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I agree with the comments above. In the US, most of these patients are eventually referred to pulmonary hypertension centers of excellence, and following a right heart cath, their treatment revolves around the use of sildenafil, CCB, anticoagulants, prostacyclin, bosentan, etc, in various combinations, as above-aluded to. Usually, these patients are already on some type of immunosuppressive therapy, including Plaquenil, however their use is not necessarily directed at or dictated by the PH bur rather at the underlying inflammatory disease, 
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I am planning to perform some studies to assess the immunological profile of my purified natural compounds esp. their role in type 1 diabetes, i.e. autoimmunity. It will be great if you can share with me the assays which can be performed. I was thinking of migration assay, FACS, luminex and others.
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Check this thread where a number of databases addresses are given. You can search these databases for the biological properties of your test compounds and their assays through the references.
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I found research on the TIMP1/MMP9 and 1) MS 2) SLE and 3) Bullous Pemphigoid 4) Rheumatoid Arthritis 5) Autoimmune Encephalomyelitis 6) Autoimmune chronic active hepatitis 7) Sjogren's syndrome 8) Systemic sclerosis 9) Autoimmune-mediated dysthyroidism 10) Polymyositis 
Im curious if anyone has found TIMP1/MMP9 to be involved in other autoimmune diseases
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Dear Joshua,
in ANCA associated vasculitis it was shown that TIMP1, MMP3 and MMP9 are abundantly regulated in active disease and decrease after induction of remission.
Andreas
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Alternative medical practitioners love to make this claim, as seen in many YouTube videos. 
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I am not aware of any reason to think this. Indeed there is no reason to think that micro-organisms have much to do with autoimmunity. I think one might as well ask if there is any reason to think RA is due to eating bananas. Unfortunately pseudoscience and gossip plays a large part in immunological theory even within high profile journals these days!
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I dont understand why i always got higher expression of healthy subject than the patients it self. This time we use autoimmune patients. My control subject ( healthy subject) is always get high expression of M3R elisa. Do you have experience about this M3R Elisa (peptide) ? 
We compared it using 7 peptides ,  we mixed peptide 1-3 than loop1 , loop 2 , loop 3 and negative peptide.  but we got control sample was  higher than the patient`s..  Can you explain about this? 
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The ELISA you use may not be sensitive enough to detect accurately M3R in blood (what fraction do you use?). What you call high expression relative to values for the patients may still  be close to the lower detection limit (do you have a standard curve to refer to?). I have never used these particular ELISA but I know that some other commercial  ELISA do not always work well when used with patients' samples. The following reference may help you: Ann Rheum Dis 2011;70:235-236 doi:10.1136/ard.2010.129049
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There's an interaction with a protein, FAP2, on a bacteria, F. Nucleatum, with TIGIT on natural killer cells. I want to target the natural killer cells specifically to block this interaction between the bacteria and the NK cells. I wanted to insert an antibody in mice transgenic for human TIGIT, however if I do so this will elicit an auto-immune response. How can I get around this? I'll consider alternative approaches outside of targeting FAP2 and/or the bacteria.
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You can make F(ab')2 fragments of your antibodies - there are lots of protocols for this available, but the most common way to do it is add pepsin for a few hours to cleave the Fc portion of the antibody. This will still block the receptor, but without the Fc portion it won't activate complement or Fc-receptor-mediated responses. This assumes that your antibody is a blocking antibody, and if you are not sure of this then you should test it in vitro first.
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I'd like to perform an experiment on mice inducing EAE with whole myelin as the immunogen. The most important reference seems to be "Oct;21(4):749-57.
Myelination in rat brain: method of myelin isolation. Norton WT, Poduslo SE.J. of Neurochemistry 1973" that obviously is about rats.. Thank you in advance for your help.
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Just a few simple pratical suggestions.
For an optimal immunization animals must receive an intradermal injection of the antigen in a depot form that will release it slowly. For this purpose any lyophilized preparation must be reconstituted in water or in saline solution up to the appropriate concentration and the suspension must be emusioned with Complete or Incomplete Freund's Adjuvant until a thick compound similar to a cream will be obtained. This is usually carried out connecting two opposed syringes with a two/three way connector one containing  the Freund's adjuvant and one the water/saline suspension (a connector can also be built in house, connecting a  large caliber needle with the cap of a secon identical needle). Pumping grdually the water solution in the oil a nice thick emulsion will be easily obtained. The thickness of the emulsion is critical for a efficacy of the depot.
Animals can be injected in the foot paths or in the skin around shoulder or hind limb joints, with  insulin syringe and needle. There isn't much room for large volumes of emulsion in these sites, therefore the concentration of the antigen in the emulsion must be carefully planned in advance.
Purification of Myelin from brain or spinal cord is simple, all the methods are based on gradient centriugations. In addition I believe that at least bovine and mouse purified  myelin prparations can be purchased from the market.
However, as already suggested by others, fresh brain white matter or spinal cord, whatever the source, will work nicely as well. In this case fresh tissue can be lyophilized and stored or can be used as a fresh preparation. If used fresh it may not be necessary to dissoleve it in saline solution
Best regards, and good luck with your experiments.
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A middle aged woman with past history of ear discharge has bilateral pneumonia and nodules on CTchest,  she has active urinary sediment and proteinuria,her ANA is -ve, but anti ccp is strong positive,she has leucocytosis,thrombocytosis and raised ESR, there is no arthritis at the moment but gives history of arthralgias in past ~10 years.I have sent her ANCAS , they are awaited
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Anti-CCP can be found in all diseases....even OA...but they are more specific (75-80%) for RA.
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Is anti neuronal antibodies is exclusively found in cancers?
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Why not ? Autoantibodies are comonly an epiphenomenon not only in autoimmune diseases, but sometimes temporarily in imunopathological conditions as a sign of increased autoimmune activity of immune response, which could be physiological.