Questions related to Immunity
Immunity rules have always been quite controversial. Many scholars believe that to grant immunity to eg, Head of State or other state officials goes contrary to the fundamental principle of justice and human rights, especially if those state officials are charged with crimes of jus cogens status.
So, does this mean, immunity should be denied as a defence to charges involving of allegation of crimes of jus cogens status (eg, genocide, crimes against humanity etc) regardless of the national or international character of the jurisdiction concerned?
After some research, I have learned that if two parties at disputes are two states, then the other state always has to respect the immunity of the other state (due to the principle of state sovereignty and equality-eg, Arrest Warrant Case). But eg, if an arrest warrant was issued by the International Criminal Court, the answer will be different. Al Bashir Case showed how the ICC denied immunity as a defence by getting around with Art. 98 of the Rome Statute.
One reason for posting this question is to hope that by following this question it is possible to keep up on developments pertaining to this question.
An article in a health magazine, Stat, by Sharon Begley, Experts envision two scenarios if the new coronavirus isn’t contained, suggests the answer for now is, not sure.
An article in Lancet, Nowcasting and forecasting the potential domestic and international spread of the 2019-nCoV outbreak originating in Wuhan, China: a modelling study, by Prof. Joseph T. Wu, Kathy Leung, and Prof. Gabriel M Leung, remarks in the discussion portion of their paper that `independent self-sustaining human-to-human spread is already present in multiple Chinese cities’ including global transport hubs. This suggests that containing, confining and eliminating COVID-19 as a pervasive and ongoing infectious disease might not be possible.
If infected people do not acquire immunity, that affects calculations of the ongoing spread of COVID-19. For example, if 70% of a population catches COVID-19 and most survive and acquire immunity, then the size of the group that COVID -19 could newly infect would be smaller. In that way, over time, as the number of people who survive the disease increases, the rate of new infections might decline because there would be fewer people without acquired immunity. I wonder what epidemiology says? These issues also affect hopes for a vaccine.
Regardless of what the immunity situation is, it seems to be that there should be a permanent cultural shift away from greetings such as handshakes and kissing.
Vertigo is a condition that can make it feel like you or your surroundings are spinning, sometimes leading to a loss of balance, according to the U.S. National Library of Medicine.
Coronavirus 2019 or COVID-19 is a novel entity which had led to many challenges among physicians due to its rapidly evolving nature. Vertigo or dizziness has recently been described as a clinical manifestation of COVID-19.
So, Are dizziness and vertigo COVID-19 Symptoms? and why?
Dear RG community,
As far as I know, antibodies are different in vaccination and natural infection. While natural infection produces antibodies against different parts of the virus, vaccination produces antibodies against only parts of the virus that are present in the vaccine. For instance, nucleocapsid proteins are not present in the vaccine, so antibodies are not produced against nucleocapsid proteins by vaccination. Is there any authorized COVID antibody test to differentiate a person’s immunity as either natural infection or vaccination? (For instance, a person gains immunity from vaccination not a natural infection, or a person gains immunity from vaccination 70% and natural infection 30%, etc.)
On the other hand, both vaccination and natural infection can produce the same type of antibody. For example, both vaccination and natural infection trigger to produce antibodies against spike proteins. Is there any difference between these two proteins? Can we differentiate antibodies against spike proteins that are triggered by either vaccination or natural infection?
Plan to add a tag with the GOI for the protein-based vaccine. Are there any tags or certain short AAs that can activate the innate immune response?
Immunity can be defined as the first defense line for the body against a lot of infections especially what is known by now as coronavirus infection. So, we need to boost that system in order to make us safe or at least less exposed to catch the disease. How can we do this properly?
Are resistance (R) genes expressed in response to pathogen attack - or only defense genes - as part of the plant immune response? R proteins act as receptors to recognize pathogen effectors and an interaction between R protein and effector stimulates Effector Triggered Immunity (ETI) which itself involves the expression of defense related genes. However, are R genes also expressed as part of ETI?
In your opinion, which country is most successful in control over COVID-19 spread so far? Please share the reasons in favor of your choice.
RNA vaccines follow a different strategy, without using any "real" component of the virus at all. Instead, researchers aim to trick the human body into producing a specific virus component on its own. Since only this specific component is built, no complete virus can assemble itself. Nevertheless, the immune system learns to recognize the non-human components and trigger a defense reaction. So May I ask, What are your opinions about the safety and efficacy of the BNT162b2 mRNA Covid-19 Vaccine?
According to recent study showed that Nicotine may play an indirect role that makes it harder for the virus to gain to access cells AND smokers seem less likely than non-smkers to fall ill with COVID-19.
What is your opinion ?
In my opinion : Nicotine is known to decrease immunity response against infections . So , possibility to develop cytokine storm will be less. I believe this is why it help in COVID-19.
The same thing you will see less aggressive COVID-19 in patients with immunodeficiency e.g. PID or patients on immunosupressive e.g. SLE and RA patients.
I need to hear your opinions regarding this issue.
Abdul Hadi Al-Qahtani, MD/MHA
We would like see the capability (possibility) of a test substance in enhancing or normalising the expression of TLR2/4. In this context what type of Invivo model or inducing (antigen/ chemical) agent is ideal to test this hypothesis ?
I want to assess the phenol-oxidase activity (PO activity) of bumblebee haemolymph. However, the protocols I found in literature always use a centrifuge step at 4°C to obtain the clear hemolymph without hemocytes.
However, our lab's centrifuge doesn't have a cooling function. Would it be a big problem to use a regular centrifuge without cooling for this step? Or does anybody know of a protocol where this cooled centrifuge step is not needed?
Thanks in advance!
Traditional varieties are doing extinct day by day in the race of high yielding varieties. Many indigenous varieties were cultivated past 20 – 50 years. How will allow again the traditional varieties in the situation of climate change? Human diet diversity was played pivotal role during forefather’s life or before 50 years past. Would it be right to say that the native varieties helped to increase immunity? In todays’ situation every person is ready to do something to increase immunity. If today we had food made with native varieties in our plate, then we would not have to run for immunity?
#Climate Change #Food diversity #Immunity #Traditional Varieties
Many countries of the world particularly United States, Germany, United Kingdom and Italy are planning to issue an immunity passport for COVID-19. How it would be implemented? Is it a good or a bad idea while we do not know when the COVID-19 pandemic will end?
Should we wait for vaccine against COVID-19 or also look towards other possible options to reduce mortality rate of Corona virus. Can Physiotherapists critically analyze the effect of exercise in Corona patients as exercise has cardio-respiratory effects as well as influence on Immunity.
Need your help and suggestions please?
According to Kirill Dmitriev, head of Russia’s Direct Investment Fund that bankrolled the effort, a vaccine developed by the Gamaleya research institute in Moscow may be approved in days, before scientists complete what’s called a Phase 3 study. That final-stage study, usually involving tens of thousands of people, is the only way to prove if an experimental vaccine is safe and really works.
Scientists worldwide are sounding the alarm that the headlong rush could backfire.
I produced Glycerol monolaurate in lab scale, with a melting point of about 37 C. Now I want to use this product as animal feed additives. However the melting point of 37 makes the product difficult to be sold as solid nor as liquid. Now I need to convert this product to be liquid at room temperature, what do you suggest? Kindly put into consideration that the final product is feed additive.
One suggestion is to mix with a another material with very low melting point.
I need to obtain dendritic cells that are free of macrophages. After the Helft paper (Immunity, 42:1197, 2015), this seems difficult from BMDCs ? Even sorting out F4/80+ cells should not work, because DCs are F4/80med. So how would you get rid of macrophages in BMDCs ?
Worry less about the virus's behaviour (mutation, airborne, immunity, new strain etc) - Because experts are working on that :)
Worry more about personal behaviour - Wear a mask, wash hands, avoid public place and crowds.
We need to focus on what's in our control and keep our lives cautiously.
Can anyone discuss the claimed efficacy of COVID-19 vaccines (e.g., 80%, 95%, etc.) by different manufacturers (COVAX, Pfizer or others)?
The reason why is they have specific immunoglobulin to covid-19 since in their past having contracted common colds due to many strains of coronaviruses, they have crossreactivity so they become also immune to the covid-19.
Related 5 websites articles are below:
SMOKERS CONTRACT COVID-19 SIGNIFICANTLY LESS AND MILDER!
Related 5 websites articles are below:
WHY SMOKERS CONTRACT COVID-19 SIGNIFICANTLY LESS AND MILDER?
Most probably, since smoking is chronic inflammatory process in nasal mucosa and also smokers most often smoke outside or by an open window they contract much more easily common cold and often their mucosa. Due to these multiple contractions of common colds, they have antibodies to both coronaviruses and rhinovirures which are the most etiologic viruses in common cold (coryza) cases. Due to cross reactivity of coronaviruses antibodies they are considerably immune or resistant to covid-19. These coronaviruses antibodies cause significant loss of smelling also. More common colds and less smoking simply means more immunity to covid-19.
Immunity is the ultimate hope in this pandemic. I just wanna to know antiviral immune response in the body. Please suggests some paper which elaborate the mechanism of antiviral response. Thanks in advance.
Aswagandha (Withania somnifera) is a well known herb which has many medicinal properties. What are the roles of Aswagandha to Boost Immunity?
Are there any reports on the correlation between the consumption of oseltamivir(Tamiflu) and the incidence or mortality of COVID -19 patients?
what is the effect of Tamiflu on immune system?
Almost all the microbiology textbooks and relevant research articles mention that Hepatitis B core antigen is not released into the blood of the host. It rather interacts with other core antigen particles to assemble the capsid of the Dane particle. My question is then how the body produces antibodies against HbCAg?
In the COVID-19 infection, the main issues are not brought by the virus itself, but by our bodies' excessive immunological response to the infected organs - the cytokine storm. This cytokine storm destroys all cells near the focus of infection and kills the respiratory system. So is there any natural non-aggressive way to prevent the cytokine storm from happening in the severe COVID-19 cases?
Thank you in advance for your valuable opinions!
Sleep is known for its immuno-modulatory and immune strengthening effects. Different sleep stage specific deprivations studies across animal kingdom are found correlated with many patho-physiological, immune-weakening and health detrimental issues. Is the lack of sleep with modern stress and socio-economical changes are driving the immuno-deficiency in humans to combat virus challenges?
This question relates to the question, Is it possible to catch COVID-19 twice? Acquired immunity might slow the spread of COVID-19 or provide some protection from re-infection for those who survive the disease. The advantages of acquired immunity might be impaired if the rate of mutation, or the kinds of mutation, impair the advantages of acquired immunity.
A March 3, 2020 research article in the National Science Review considers mutation: On the origin and continuing evolution of SARS-CoV-2. The authors are: ang, Xiaolu and Wu, Changcheng and Li, Xiang and Song, Yuhe and Yao, Xinmin and Wu, Xinkai and Duan, Yuange and Zhang, Hong and Wang, Yirong and Qian, Zhaohui and Cui, Jie and Lu, Jia.
The article describes two major strain designated L and S. The authors infer that the S type is the ancestral version, and is less aggressive. The L type they said is more prevalent, about 70% than the S type, about 30%.
The public health advice to follow social distancing is directed to slowing the proliferation of the disease. But I wonder: might social distancing also impair the mutation rate of COVID-19? If slowing the mutation rate is beneficial, then social distancing has advantages in addition to slowing the spread of the disease. Do you know the epidemiology that relates to this question?
Is there any reports on the correlation between Vitamin C status and incidence or mortality of COVID -19 patients?
Are there any reports on the correlation between Zinc status and incidence or mortality of COVID -19 patients?
In our experimentation, end point is quantification of NK cells after treatment period. Different markers like CD25, CD69, CD16 etc., were given In literature (there is no uniqueness in marker selection for quantification of NK cells). So, here my basic doubt is, what is basis / rationale to select the marker for the quantification of NK cells and what is ideal marker for the same?
I would like to know a good adjuvant to combine with some peptides of 20aa long to immunize rabbits and after recovery of antibodies.
I'm looking for assays where I can track single cell - single bacterium dynamics, mainly rate of killing. Most methods I find online revolve around finding a single infected cell and following it via live cell microscopy. Are there any other methods, where I can follow the course of infection in a single cell, such that I can measure bacterial killing/survival in macrophages? Thanks!
Values above 7 can be considered ok? I made the RNA extractions using TRIzol.
I want to quantify the expression of some immune genes in spleen and head kidney of bacterial infected fish. I also tried to extract total RNA from the liver and muscle, but several samples are RIN N/A. Is it necessary to use the TissueLyser for these organs?
I am trying to find the list of cells that content endosomal TLRs (TLR3,7,8 and9). Are these TLRs expressed all over the body or there are very specific cells that expresses these TLRs?
Any input is appreciated. Any reading material to find the answer is appreciated.
I am screening products against PBMCs, testing for potential immune activation. I have been looking at CD69 as a good general marker of immune activity, but would prefer something secreted. Does anyone have some good recommendations? Thanks!
I've been (not so successfully) trying to perform basic experiments on dendritic cells to analyze the actions of a fatty acid. I've noticed there are numerous methods to do this and it seems that many people use completely different methods to arise at the same population. I've tried a variety of these methods and have not obtained similar results.
For example, I first tried isolating BM cells (femur flush) and treated them with GM-CSF and IL4 at 20 ng/mL or 10 ng/mL for 5-10 days. I never reached a CD11c% > 60. I've tried taking the adherent cells. I've tried taking non-adherent cells, and now I'm going to try obtaining both. These methods are routinely published and groups get >90% with or without positive or negative selection with beads. It seems that 50% of papers will actually publish the flow results for the DCs before they use them.
Meanwhile Helft et al. 2015. Immnity 42 demonstrated that even CD11c+ cells are 50% macrophages and not DCs. These data were debated (Helft Immunity 2016, Guilliams Immunity 2015, Lutz Immunity 2016) but there still was never a general consensus. More recently, a paper published in J Immunol (Jin and Sprent 2018) demonstrated even newer methods that yielded greater amount of DCs by using less cells and adding IL4 late during culture.
For someone new in the DC field this is very confusing and it seems that there is no tried and true method to isolate DCs. Is the CD11c+ count all that matters? How many markers do I need to show are active upon stimulation? Is CD80/CD86 enough? Do I need to show CD115, CD64, CD24? If so, this is barely ever done. Many groups also just say "We isolated DCs as done previously". This is great except it cites papers from nearly 20 years ago.
I am sorry for the long-winded questions but any help/direction would be very much appreciated!
Good morning all,
I was wondering if it's possible to use CIBERSORT (or similar deconvolution algorhitm) on RNAseq data of gut biopsies from humans?
We are trying to gauge the presence of immune cell types in them, but the biopsies also contained epithelia, fibroblasts and other cells. I am worried that using the LM22 signature set will give me bias due to many transcripts coming from these non-hematopoietic cell types. Based on what I understand, this should be possible, right?
Second part of my question, we get quite high (insignificant) deconvolution p-values. Is there any way to improve them?
My example outcome attached.
Thank you very much for your time,
I would like to quantify the activation of cell surface antigens, in this case CD69, on peripheral blood mononuclear cells (PBMCs) to screen for an immune response. Do I need to take any special steps or precautions, such as lysing the cells, since the antigens are found on the cell surface, instead of being secreted into the media?
Small and large intestine are different organs, but have similar structures and functions, here I want to ask,
1) As for intesitnal immunity development, it seems that small intestine contains more immune cells than colon, so small intestine contributes more to intesitnal immunity development?
2) Do small intestine and colon share immune cells? through what mechanism?
The differentiation protocol of mouse CD34+ bone marrow cells into dendritic cells is well known. Is anybody familiar with protocols describing the differentiation of mouse CD34+ BM cells into other immune cell types (e.g. T and B cells, NK cells, etc.) ?
For example, measuring lymphocytes conc. in control gp was 100 ug/ ml while group 1 average was 115 ug/m, performing student t test results were signficantly different. But how to explain this in terms of fold change?
Is expressing the results in terms of fold change a must to prove that there was an improvement (increase) in the group than the control?
Once triggered into action, an immune cell overhauls its metabolism, making changes that could be exploited for treatment.
I was told that survivors of tetanus do not generally acguire natural immunity to the disease. However, does it happen at least sometimes? Or, if not imuunity, do they have tetanus antibodies after they survive the disease ? Obviously, I mean the circumstances when nobody gives them a toxoid booster.
It has been shown that the treatment with ruxolitinib, which selectively blocks JAK1/2-dependent signaling pathways, resulted in a high response rate exceeding 80% among corticosteroid-refractory GVHD patients.1 It is notable, however, that IL-2-JAK3-STAT5 axis is also considered to be responsible for the therapeutic effect of ruxolitinib. IL-2-JAK3-STAT5 axis is essential for the development, survival, and proliferation of regulatory T cells (Tregs).2 The conversion of FoxP3-negative Treg-progenitor-cells into mature FoxP3-positive Tregs in the thymus occurs mediated by TCR-independent but IL-2-STAT5-dependent process.3 Ligand binding by the high affinity IL2-receptor complex results in the phosphorylation of three key tyrosine residues localized in the cytoplasmic domain of IL2-receptor-beta by both JAK1 and JAK3.2,3 Furthermore, it has been also shown that ruxolitinib suppresses the differentiation of donor T-cells into Th1/Th17 cells, while increasing the differentiation into FoxP3-positive Tregs.4 Importantly, ruxolitinib is reported to inhibit IFN-gamma signal transduction in donor T-cells, which is required for those cells to infiltrate into GVHD target organs via chemokine receptor CXCR3.5
1: Zeiser R, Burchert A, Lengerke C, et al. Ruxolitinib in corticosteroid-refractory graft-versus-host disease after allogeneic stem cell transplantation: a multicenter survey. Leukemia. 2015;29:2062-2068.
2: Mahmud SA, Manlove LS, Farrar MA. Interleukin-2 and STAT5 in regulatory T cell development and function. JAKSTAT. 2013;2:e23154.
3: Burchill MA, Yang J, Vang KB, et al. Linked T cell receptor and cytokine signaling govern the development of the regulatory T cell repertoire. Immunity. 2008;28:112-121.
4: Spoerl S, Mathew NR, Bscheider M, et al. Activity of therapeutic JAK 1/2 blockade in graft-versus-host disease. Blood. 2014;123:3832-3842.
5: Choi J, Ziga ED, Ritchey J, et al. IFNγR signaling mediates alloreactive T-cell trafficking and GVHD. Blood. 2012;120:4093-4103.
Dear Sir/ Madam,
I am doing research on feed additives (prebiotic, probiotic and synbiotic) for fish and need a clear very concept about pro-inflammatory cytokine genes (TNF-α, IL-1β, and IL-6) expression. From internet and some researcher working on cell culture said “if the relative expression level of pro-inflammatory cytokines is higher than control means inflammation is in the body which is bad for immunity” and they thought feed additives will be used for decreasing the relative abundance of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6). However, my research result showed opposite of their thinking and the following 1st three articles showed significant higher expression and 4th one showed significantly lower expression is good for fish immunity.
1. “B.T. Standen, M.D. Rawling, S.J. Davies, M. Castex, A. Foey, G. Gioacchini, O. Carnevali, D.L. Merrifield, Probiotic Pediococcus acidilactici modulates both localised intestinal-and peripheral-immunity in tilapia (Oreochromis niloticus), Fish. Shellfish Immunol. 35 (2013) 1097–1104”
2. “A. Abid, S.J. Davies, P. Waines, M. Emery, M. Castex, G. Gioacchini, O. Carnevali, R. Bickerdike, J. Romero, D.L. Merrifield, Dietary synbiotic application modulates Atlantic salmon (Salmo salar) intestinal microbial communities and intestinal immunity, Fish Shellfish Immunol. 35 (2013) 1948–1956”
3. “A. Panigrahi, V. Kiron, S. Satoh, I. Hirono, T. Kobayashi, H. Sugita, J. Puangkaew, T. Aoki, Immune modulation and expression of cytokine genes in rainbow trout Oncorhynchus mykiss upon probiotic feeding, Develop. Comp. Immunol. 31 (2007) 372–382”
4. C. Qin, Y. Zhang, W. Liu , L. Xu, Y. Yang, Z. Zhou, Effects of chito-oligosaccharides supplementation on growth performance, intestinal cytokine expression, autochthonous gut bacteria and disease resistance in hybrid tilapia Oreochromis niloticus♀× Oreochromis aureus♂, Fish shellfish immunol. 40 (2014) 267-274.
If anyone can provide, clear concept about pro-inflammatory cytokine expression and its relation to immunity will be very much helpful for me. If you have any good document please send that to me.
Thanks in advance..........
Immunoglobulin class switching, also known as isotype switching, isotypic commutation or class-switch recombination (CSR), is a biological mechanism that changes a B cell's production of immunoglobulin (antibodies) from one type to another, such as from the isotype IgM to the isotype IgG.
#space #iss #humanspaceflight
Hi Dear colleagues, We want to know which herbal extract may have efficient effect to increase antibody production and immune response in fish were experimentaly i.p. injected with a vaccine containing bacterial lysate plus herbal extract
Hello Everyone! I wanna make some actuators based on PAMPS gel. I am not chemistry backgroup. So what I can do is just buying PAMPS water solution on Sigma-Aldrich and trying to cross-link it. I saw various crosslink method on papers. But I am not sure which one should be the best one for actuator application. Could anyone of you give me some advice or references? Thanks a lot!:)
My lab would like to perform an immune cell killing assay using activated T cells or PBMCs on miRNA treated ovarian cancer cell lines. Ideally, we could like to see if there is a difference in immune cell induced apoptosis of the cancer cells between treated and untreated cells. However, as a lab we have no experience in working with immune cells so it would be great if someone could highlight the important points to consider while designing such an assay.
Thanks in advance
Hi, I am doing an adoptive transfer study in which I transfered splenocytes from immunocompetent to immunosuppressed mice. I am wondering, for those with experience, how long does it take until you see the transfer to take effect?
I am going to use Immune complex for testing my antibody binding to FcgRIII on NK cells. The immune complex consists of the whole virus. But I want to get rid of unbound antibodies from IC solution. Has anyone used MWCO columns for getting rid of free antibodies? What KDa? And what company?
I am currently looking into reviving T-cells or B-cells from frozen human tissue. Is it feasible? If yes, is there a specific way on how to freeze the tissue in the first place to get the best possible outcome?
This is for immunotherapy-based studies, so in general how a human tissue sample can be stored?
Thank you in advance
Can anyone suggest me the suitable normal cell lines to study TLR immune pathway? The cell lines that can produce the cytokines?
Perhaps this is a stupid question but it came across my mind that it is much easier to evade immune recognition of antigen derived from immune privileged sites such as the brain, the bone marrow and the placenta. How do these sites not having higher chance of developing tumor than other organs? Please share with me your idea. Thanks so much
I wonder whether anybody has been able to detect exosomes from an MHC knockout/knockdown lymphoma cells(or any kind of immune cell line) or not?
I recently identified significantly increased levels of phosphodiesterase type 5 (PDE5) in the serum of sick patients relative to normal control patients. While I think this is interesting, I have little experience with phosphodiesterases and am wondering why this would be increased? What might it be doing in circulation? and how is it released? I'm trying to gain an idea about whether or not this is relevant to study, given that I am a new postdoc!
Stick floating cells to glass cover slip, any specific reagent, their concentration, and your experience.
I am trying to identify submucosal immune cells in samples of rat gut tissue via IHC, but need a good marker/antibody for these cells. Does anyone have any suggestions as to which marker may be appropriate? Thank you.
I know experimentally the percentage of CD4, CD8 and NKT cell equivalents I 'm getting from my guinea pigs but would like to know if it is comparable to murine and human, or if substantial proportional differences exist.
Is there any data on Rhesus prophylaxis for women with weak or partial D types?
Which weak D types would be in danger of immunization, and how much Anti-D (dosage) should they get, as their red cells will surely react with the antibody?
What do you do?
Generally a lysogen will protect the bacteria from a super infection by a similar bacteriophage. However does this immunity extend beyond the family level ? Is anyone aware of any example ?
Have come across a strange lagged response to an infectious agent where females seem to respond far more rapidly than males.
Is there anything in the literature regarding profound differences in immune response between the two genders or anything about gender and immune lags or immune feedback loops?
I want to study the relation between the dose of antigen and liver immune status.But I don't know how to judge the live‘s immune status.Is there a criterion that differentiate liver’s immune status？
Why cannot we use an algorithm of physical means - temperature, pH, salinity, pressure etc, and even time - which is survivable by every human cell type but unsurvivable by pathogens? The big question is not how to create these conditions within the body, but would it work, if we could create them?
So far I haven't found anything in the literature to tell me why this would not work.