Questions related to Autoimmunity
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.
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
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?
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?
Is there a certain boundary between immune-modulating and autoimmune response in case of COVID-19? What is your opinion?
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.
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?
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.
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
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.)
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.
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?
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?
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?
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).
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?
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.
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.
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?
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.
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)?
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.?
Subjective experience in a hot near-desert climate with extremes of hot and cold temperatures during the year
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
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.
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.
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?
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?
Antibody-testing in Susac syndrome - antigen target and availability of analyses.
I am noticing though subjective, a substantial number of autoimmune conditions in a Northeastern Nigerian location, hot quasi desert climate
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?
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.
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.
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!
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?
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.
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?
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?
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.
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?
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.
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 ?
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?
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.
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
- How long would you expect auto-antibodies to be present in CSF in autoimmune encephalitis?
- Would there be any difference between untreated and treated (IVIG/rituximab) cases?
- 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!
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.
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?
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?
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 .
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?
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?
Why hydroxychloroquine can treat primary ITP with positive ANA antibody and can't if it is negative? and what is the evidence?
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?
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.
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.
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.
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
Alternative medical practitioners love to make this claim, as seen in many YouTube videos.
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?
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.
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.
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