Are there any excellent lecture series available online? Free to follow? Nothing from MIT OpenCourseWare.

I'm looking to apply this fall for an immunology PhD starting fall 2025. Trying to get a list together of schools to look into, and I'd love to hear about peoples experiences!

Personally, I'm most interested in autoimmune disease and thats where my current research is, but Im not married to that specialization. I'm looking for programs in the US, Canada, or english speaking europe, ideally in fairly urban areas that are possible to navigate without a car.

If you recently got/are getting a PhD in the field, could you tell me a little about where, and the pros and cons of your experience there? I'd really appreciate it! Thank you so much!

Mouse T cells are more sensitive than Human T cells, are IL2 concentration play a significant role in T cell activation via CD3/CD28? Would too much IL2 kill my mouse T cell invitro culture?

Location : USA, EU, AUS

For primary cell culture I have to combine cells from multiple mice to increase the cell numbers. I know you can pool the cells of mice with the same genotype, but would you also pool cells from male and female mice with the same genotype? For primary microglia cultured from newborn mice we do pool multiple brains (sex is not known because of the age p1-4). I am also doing primary cell culture using adult mice, so the sex is known, but it is sometimes difficult to get enough animals of the same sex and age since the mouse line is not very fertile. Can I then combine female and male cells for cell culture? I usually want to compare wildtype to knockout microglia and macrophages and I look at their response to virus and TLR ligands, including the Interferon I response. I know male and female mice respond differently to interferon signaling. However, are male and female cells more “activated” when cultured together, because of the difference in X and Y chromosomes? Thank you for your help!

I have a primary immune deficiency which has caused lifelong illness. I finally got referred to an A/I after many years. The diagnostic process started 5 years ago and remains incomplete. I saw one A/I doctor who botched the initial diagnosis, then came up with a partial diagnosis on the next visit, then incorrectly claimed there was no treatment. (And also made incorrect statements about PCR vs rapid test positivity and the prevalence of long Covid.) I got referred to a new A/I who (after a lot of back-and-forth) said she doesn't treat PIDs. She rejected the other A/I's diagnosis and said I just need to do a nasal saline rinse. (This had a real chiropractor feel to it.)

As I started asking more questions of online PID groups, I found that my experience is sadly typical.

I eventually connected to a PID expert doctor who specializes in my class of PID, and he responded:

"In my personal opinion any good allergist/immunologist (private practice or academic) should be able to manage your PID, but finding a good provider is always half the battle.  A lot of specialists are either primary allergists who are unable/unwilling to learn immunology, or they just don't care since it doesn't make money like allergy shots do."

So the problem I'm encountering seems to be well-known within the speciality.

I've seen a ton of specialists over the years hunting this down and, if anything, I've found them unwilling to speak confidently outside of their specialty. But here we seem to have a group of doctors who are confidently wrong.

[Edit: I know the internet is full of a-holes, but it's really incredible that somebody would reply to this with "factitious disorder." My experience is hardly surprising if there are people out there who want to be immunologists but hate people with immune deficiencies. Anesthesiology is right there for anyone who doesn't want to see patients who speak.]

Why do some of them have long strings of the letter b? Why are they not given more descriptive names? Why does it feel almost random? Why am I so angry about this? Biology is full of slightly strange naming conventions, which I understand. Certain proteins are discovered in one context but are found in others after their discovery e.g BNP, TNF alpha. But these are forgivable, but why on earth would you call something so robotic. This post isn’t calling for an upheaval of the naming system, which would ultimately create more confusion as people would find different names for the same thing when researching older sources.

Interesting paper I found and a (probably terrible) idea from a biology student

https://www.science.org/doi/10.1126/scitranslmed.adi1145?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed

Epitope base editing of CD45 to create a modified version that is not recognized and attacked by CD-45 targeting CAR-T cells. Scientists testing it in pre-clinical studies for use against leukemia, where CD-45 targeting CAR-T cells (which have the modified CD-45 antigen as well to prevent them from killing each other) kill the leukemia as well as all healthy white blood cells. Patients then receive a hematopoietic stem cell transplant (HSCT) expressing the modified CD-45 antigen to reconstitute the immune system.

Would such an approach be feasible in severe autoimmune disease like MS to reset the immune system? Autologous HSCT (aHSCT) has already been used against MS to try to reset the immune system with non-myeloablative chemotherapy followed by immune reconstitution via aHSCT. The approach is highly effective, albeit risky with side effects, which is why it's still in trials for MS in the U.S. and U.K. Anti-CD19 CAR-T cell therapy has also shown tremendous success while also being well-tolerated in trials against systemic lupus (most patients went into drug-free remission), employing a similar concept of achieving an immune reset by killing autoreactive immune cells. Anti-CD19 CAR-T cells are also in Phase I trials for primary progressive Multiple Sclerosis (PPMS), and ocrelizumab, an anti-CD20 mAb B-cell depleter, has been successful against relapsing-remitting MS (RRMS). Would it be possible to take it a step further though, since MS progression is driven by innate immune dysfunction as well (microglia and macrophage autoreactivity in the CNS), particularly in PPMS which has very few treatment options compared to RRMS.

Anti-CD45 CAR-T cell therapy followed by aHSCT expressing modified CD45 antigen could reset this innate immune autoreactivity present in progressive MS. While clearly very risky since you're killing and reconstituting the entire immune system, it could also be an extremely effective form of aHSCT that stops progressive MS.

Hi all,

I was hoping someone with some experience doing T cell activation induced marker assays could shed some light on my situation.

I want to do T cell activation based cell sorting of PBMCs based on expression of activation markers following a 24 hour peptide pool stimulation. Typically, this is done with 1 million cells per well of a 96-well and the final concentration of the peptides is 1ug/mL. Everywhere I look in the literature it is done this way, never more than 1M cells per well.

Well, I want to scale this up to 5M or more cells. I tried this once w 5M cells in a 96 well and the media was yellow the next day and the cells were definitely not psyched. Is it appropriate to try to scale this up? How should I scale up? My instinct is to use the same cell to volume ratio and do 5M cells in 1 mL in a bigger plate, maybe a 48-well? and do I keep the concentration the same, or scale the peptide amount to something else? It seems like it should work the same, I just want to make sure i'm not missing some important rule about T cell and APC kinetics. I've also read that the cells like to be touching each other so the APCs can interact with the Ts, and round bottom plates are preferred.

Anyone have any insight on this? Thanks!!!

I am new to this subreddit, so direct me to the right subreddit if needed. I am writing an undergraduate research paper on the potentially harmful effects of monoclonal antibodies used for organ transplant patients. I need help finding resources on this. I understand monoclonal antibodies are somewhat new as a treatment option, so maybe there isn't enough data. I would appreciate any insight on this subject or papers I can read.

Why isn't a "new allergy"...a new allergy, regardless of age? If you can treat it as a child, why can't we do it with adults? What's different that makes it possible to treat food allergies in kids but not adults? Does it have something to do with the assumption that children can "grow out" of allergies, but adults won't?

I wonder what was the first immune cell to evolve. I would imagine innate cells like macrophages were first.

Hi. About to order some B6 mice that will be used for cell transfer experiments. This will be done to track naive cells over the course of s.c. B16-F1 tumor growth. They will also eventually be bred with OT-1 mice. My question is which one of these guys should I order just for being able to differentiate transferred T cells without having to pre-label them prior to transfer. This is simply a phenotype/preference question. We used to have CD45.1 mice in my previous lab and they always looked weird compared to our WT B6 in a Th1 disease model (sometimes sicker, different cytokine expression) but that could’ve been my own hands or the lab colony itself. Just looking for weird experiences someone might have had with Thy1.1 or CD45.1 mice on C57BL/6J background. Thanks.

I've had this idea of using a CRISPR library of human genes to edit T cells in mice and then re-inject into tumor bearing mice.

Would these be inherently immunogenic? I know people make mice to express human proteins often, but my science gut tells me this shouldn't be allowed.

I understand the human version might not “play nice” with other proteins in the same way, but I’m really more interested in the T cell function and finding perturbations that would be more directly translatable to human therapies.

Any insight helps, thanks!

Why are they referred to as MHC class I (or i) and II (or ii) instead of MHC class 1 and 2?

My understanding is that natural killer cells are always circulating and looking for cells that aren't displaying MHC-I to induce apoptosis in. In other words, they don't need to be activated by any other cell? Also, I wonder what would have to happen to increase the number of natural killers being produced? For example, if they find a large tumor?

What is it that determines whether a T cell becomes a cytotoxic or a helper?

Question:

I understand that a cytotoxic T cell can be partially activated by a dendritic cell that is acting as an APC, then fully activated by a helper T cell (that itself was already activated by the same antigen). How does the second activation of the cytotoxic T cell occur, given that neither of the T cells is an antigen presenter? ... Am I missing something? ...

Hi team. I'm super embarrassed to ask this question given that I've used the tool frequently, but I'd like to know how antibodies are able to deplete cell types? I've done a lot of googling but I've yet to find the actually explanation of why/how this works. Does it have to do with opsonisation of the cell after the ab binds the target due to the species of the ab?

I'm talking about CD4 specific T cell depletion with GK1.5, for example. Literature links and/or references highly appreciated. It's just always puzzled me.

I am looking for the terminology for a specific interaction.

When a host protein that is non-immunogenic binds to a immunogenic foreign body like a viral protein or PAMP and an immune reaction occurs against that host protein being the immune system sees it as part of the foreign body what is this called?

I was thinking Hapten but that only includes compounds up to a molecular mass of 1000da not bigger.

Further, from my understanding the carrier protein of said Hapten does not perpetrate and immune reaction by itself. Whereas, viral proteins or PAMPs can.

I have read that the indicator of mast cell activity is tryptase. But I have also read that not everyone with allergies, and not even everyone with anaphylaxis, has high levels of tryptase. So I wanted to know if mast cells can choose what they release, like the way that body cells only transport certain things in and out, as opposed to sucking in literally everything around them or spitting out their entire contents. Do mast cells work like a stomach, vomiting everything, or can they be selective?

When mast cells get "sensitized", and they start reacting to lots of things, surely that's evidence that they can be selective? Because not everyone gets anaphylaxis, but there are lots of mast cell related disorders. If they were all spitting out their entire contents, we wouldn't have hay fever, people would only have anaphylaxis.

Are there other things that cause allergies, that spit out tons of histamine, and mast cells only get involved some of the time? If so, why is it called "mast cell sensitization" instead of "immune sensitization"? There's lots of intolerances that don't involve IgE/G, but aren't things like celiac or lactose intolerance, and do involve histamine. Do we know what the thing is that's sensitive? Why do we think it's the mast cell if we know that the mast cell is only rarely the culprit in allergies/pseudo-allergies?

Here's a paper from 2000 that says only half of people in an ER for anaphylaxis reactions had elevated tryptase, and it concludes that the others didn't have mast cell problems. This is what inspired the questions.

Since malaria infects red blood cells, and red blood cells don't have MHC-I, I was wondering what the human immune system does to try to eradicate this infection. Is there any way for the immune system to kill infected red blood cells? Or does it only try to attack the parasite when it is outside the cells? (Any links to relevant papers would be good too.)

I am stunned by what AI tools can do for research. Feel some can just write manuscripts and grants for you. Do other people use any AI regularly for their research? What are the tools people like?

In the early part of the COVID pandemic there was a common assumption that contaminated hands touching the mouth and nose could cause respiratory viral transmission, did anyone ever test this as an experiment? Clearly, touching the mouth sounds more plausible for gastro-intestinal pathogens than respiratory pathogens. Did anyone do an experiment using the inhalations of an infected humans to contaminate hands, then touch the nose and mouth of a mouse/rat/ferret or other human to see if this took place?

I understand that interferons are released by various immune cells, but does a cell that is infected release interferons? If not, what does it release to alert others that it is infected?

hi, just wondering what software do people use for spectral flow analysis? I want to generate u map like graphs with distinct cell populations. Is there something similar to Beckman's cytobank platform?

Looking for open PhD positions in Europe in the field of immunology, infection biology, cancer biology or molecular biology. Any links or advice would be highly appreciated!

Hi everyone, I want to establish an assay with Staphylococcus enterotoxin B (SEB) and I am trying to find information about which T cell receptor subsets can be activated with it and which ones not. I found some conflicting information from the papers I found so far and I am a bit confused. Can anyone help me find a reliable source of information about this? Many thanks.

if you took a neutrophil from a human, another from a monkey, and another from a mouse, and showed them to an immunologist without labelling them, would the immunologist be able to tell which one is the human neutro and which ones aren't? how different are they from one another?

My husband is almost done with his PhD in immunology, and we’re exploring options for his post-doc. His goal is to PI in a research institution afterward. I would love to live in Europe for a few years, but he says post scientists come to the US for their post-doc, not the other way around. Are there any academics here who post-docced in Europe? What was your experience like?