Hi,

I've had several instances personally and also recall several of my friends healing off a flu or cold within 5 days. How is this possible if: 1. according to my knowledge you need an antibody response to clear off an infection 2. an antibody response is a slow response to an antigen - if I remember correctly it takes approximately 2 weeks.

Can the innate immune system deal with an infection to the point its no longer causing disease?

title.

I’m defending this week and my family is kind enough to tune into the livestream. Many of them last took a biology class in high school or college decades ago. Do you have any recommendations for a good resource/overview of the immune system that I can send them? My research is in antigen presentation, so I was planning to send them the figures from Rock et al 2016, but that still presumes they know what a T cell is.

Hey, how do immunologists deal with seeing so much misinformation shared around the internet and in reddit in particular in regards to vaccinations and other immunology related fields? Do you feel the need to constantly inform others an call out the misinformation or do you just see it and not react? I find it difficult to see others fall for the same false narratives daily but feel like there is no way to argue with people who 'don't believe' or don't take the time to actually do any research into the real science behind their beliefs

I was looking up the etymology and don’t really understand the naming here

On an exemplar exam question, my professor said to assume that I eluted the peptides from the binding cleft two HLA proteins and ran them through mass spectrometry, resulting in the table below, and that “the peptides in each group were aligned to emphasize common motifs”. I understand that the letters represent amino acids but beyond that I am clueless as to how to read this table - like, what would I even google to find info on how to read this? I thought maybe it was like a map but then how could they realign it and it still tell you anything? I have a pretty weak background in advanced science stuff (I wandered into this class from a graduate health sciences program). I suspect the highlighted regions are the 1 and 2 regions that give the molecule its “self” character, but past that I’m lost, and unsure how to educate myself.

Spent some time reading up on T-cell exhaustion—the phenomenon where T-cells get ‘worn out’ in chronic infections and cancer. It’s like an immune system burnout. Fascinating to think that restoring these cells’ function could unlock better treatments for persistent diseases. Anyone else following research on T-cell reinvigoration therapies? Would love to hear your thoughts on promising studies!

Link to learn more: https://www.cancer.gov/news-events/cancer-currents-blog/2019/t-cell-exhaustion-immunotherapy"

#Immunology #TCells #ImmuneHealth #Research

Will graduate soon with a PhD in neuroimmunology after 8 years.

I am quite burnt out by academia and have no intention of becoming a professor/PI. I also don't particularly want to go into a postdoc.

Looking for industry jobs, I was quite shocked that most positions ask for minimum 2-8 years experience AFTER graduating PhD to qualify for research scientist positions. And the few positions that don't require postdoc experience have quite a low salary (for a PhD) of usually $60,000-80,000.

Personally, I would be interested in clinical/translational research, but without the pressure of academia (ie, I don't want to do research purely to just publish papers). Are there hospital/university research positions for PhD holders to do such work (and get a decent salary)?

I understand from the market approved drugs that there are quite few pure co-stimulatory pathways inhibitors for autoimmune diseases. It seems it is CTLA4-Ig fusion protein (belatacept and abatacept) and CD40L blockade seems to be doing pretty well after solving the issues with thrombotic complications etc.

How come co-stimulatory pathway is not that common to target in comparison to cytokines etc? I mean, the source to many of autoimmune (and inflammatory) diseases are cells and not really single cytokines.

Is it side effect issue? I assume one thing would be to consider that the patient should still be able to mount an immune response to viral and tumor antigens.

I got curious to know more about immunology and I bought the Janeway book. I’m currently at the complement system and God is it hard to understand what’s happening.

I understand the three pathways but there are so many biochemical details, like what type of acid they recognize on gram positive bacteria, to ficolins binding to acetylated carbohydrates and so on.

I don’t understand a lot of these biochemical reactions or their names and I get stuck googling what those are that it kinda kills the mood of reading further.

Apologies if this may be a stupid question; it popped up in my mind randomly from reading another reddit post. Hypothetically speaking, if you were to for example take a normal, healthy adult with no prior diseases, allergies, etc. and then isolate him in a closed off room (giving him enough food and water daily) for a really long time (say multiple years) and then let him out into the real world, would he be more susceptible to diseases? Could this person randomly develop allergies or asthma?

edit: changed the years, I didn't mean 1 year specifically

Hi,

I'd like to stimulate HCT116 cells with IL-1B and observe the phosphorylation status of my protein of interest. I'd need a positive control to show my IL-1B drug stimulation works. Does anyone know a bone fide readout? Preferably some proteins or phospho-proteins I can probe using western blot?

Thanks!

Not entirely sure this is the right place to ask this but I'm really curious to see if anybody knows the answer to this. I've just been wondering this for a long time and haven't really been able to find any answers. My parents lived in the Cook Islands for two years about 22 years ago. They spent the majority of their time in Atiu, as well as a few months in Raratonga. They've always told me that they absolutely could not eat any fish or shellfish out of the ocean, because the locals told them that they were contaminated with something that could potentially give them a seafood allergy, which was sometimes but not always temporary. Apparently they saw it happen to somebody they knew.

Is this a thing? I've never heard of acquiring an allergy that way, and I haven't been able to track down any literature about it. I imagine it could very well be something else like a parasite or toxic algae or something, but figured I'd at least start here.

Hi all,

For my project I want to make a knockdown of a specific cell surface protein on human primary lymphocytes derived from peripheral boood. In literature i read that primary lymphocytes are tricky to transfect. From what i gather lipofectamine RNA imax seems to be most promising. Does anyone have recommendations regarding setup (amount of lipofectamine, sirna, duration of transfection, etc) for primary suspension cells?

Thanks!

I’m due to complete my PhD in immunology (specializing in next gen vaccine strategies). Seeing as the future of vaccines in the US seems a bit rocky, especially federally, would an MD or DVM help diversify my career opportunities in a beneficial way?

I’m interested more in research, but I’m not opposed to working clinically. I currently work on both animal and human vaccines. I am just wondering if dual degree holders enjoy their work or if there are cons besides having to go to class for 4 more years?

Hello everyone my lab received patient blood today that was rotating for about 18-24 hours overnight. When we did the FICOLL purification when we isolated the PBMC layer from the gradient it completely coagulated into a gelatinous mess with a small pellet at the end. The consistency was that of thick egg whites and even the strongest setting on an automatic pipette couldn’t pick it up. It was almost the consistency of jello. At the very end there was a thick pellet of the PBMC cells. Is this some kind of contamination of a fungi? Did the combination of two chemicals precipitate? Is this a side affect from leaving the blood over night? The neutrophil layer was completely normal and had no issues. I attached the photos of the glob.

Forgive me if this post doesn’t fit the theme of the sub. I will be finishing up my postdoc tenure in early 2026 and about to start looking/applying for jobs. Just that I have no idea where to begin. My search at this moment is constrained by my visa status till my green card gets approved. Anyone been in the same boat? Any guidance would be greatly appreciated:)

I've read this article

Malley, R., Lu, Y. J., Sebastian, S., Zhang, F., & Willer, D. O. (2024). Multiple antigen presenting system (MAPS): state of the art and potential applications. Expert Review of Vaccines, 23(1), 196–204. https://doi.org/10.1080/14760584.2023.2299384

As I understand it, the vaccine is administered and Antigen presenting cells uptake it to present larger protein epitopes to B-Cells and peptides to T-Cells.

So, here is where I get a bit confused, is there a limit? 24, 30, why not 100. is there a biological process that mitigates response to avoid Hypergammaglobulinemia. Any other drawbacks to this kind of vaccine?

Thanks in advance!

Hello! I have three questions for you. Amy guidance would be well and deeply appreciated!

How do developing B cells tell between self and auto antigen when going through the auto reactivity checkpoints in bone marrow and spleen? Do they even differentiate? Wouldn’t they need to? Everything I read is just “antigen specific”, but I beg of you, which antigen???

Test for auto reactivity, soluble self molecule binds to receptors, cell enters state of anergy. Why anergy? What’s the point of this slightly autoreactive B cell to continue to exist, why not apoptosis?

Essentially the same question for soluble weak self antigen reactivity - why continue existing? It enters a state of immunological ignorance, but could still be causing autoimmune problems down the line given the right conditions, so why continue living for this cell type??

Thank you so much for any and all information!

Hello everyone,

I have synthetic chemistry background, can handle basic cell experiments. In my current project I want to use dendritic cells and bone marrow derived macrophages and observe their maturation and M2 to M1 polarization under my nanoparticles treatment. I have no knowledge of handling immune cells and their maintenance. Please enlighten me with your expertise and suggest me protocols or research articles, where and how to begin with. Thanks a lot for the help.

Since most antibodies that are transferred through breastmilk are IgA, does a mother's body produce extra IgA antibodies while she is breastfeeding so that they will still be present to protect her? What about other types of antibodies?

It seems to me like the transfer of antibodies through the breastmilk might leave the mother either too few available unless more are produced. Is there any validity to this thought?

Hi I'm looking to buy murine ifny and il17 elispot kits without the plates. I can't seem to find any , all the offers from either ctl or mabtech include some plates. If someone has managed to do so could you share a link or catalog number please?

I am currently applying for a PhD in biomedical sciences, and am interested in immunology and possibly neuroscience. I am passionate about an autoimmune disease that is interconnected with the nervous system. However, my undergraduate degree is in biomedical engineering, and my research has been computational in other fields (cardiovascular, gait rehabilitation). My only wet lab experience was in spinal cord injury. One of my biomedical engineering professors told me I would not get into any immunology programs due to my background being different. Is anyone able to provide insight on this?

Hi all,

I am planning on Treg suppression assay on conventional T cells and one question came up. When culturing Treg and Tconv with anti-CD3/28 dynabeads for Cell trace dilution, should the number of beads be based only on responder cells (Tconv) or should the total cells in a well including Tregs be accounted for?

E.g.

1. Tconv only condition - 10k Tconv + 10k beads.

2. Tconv+Treg condition - 10k Tconv + 10k Treg + 10k beads (or 20k beads)

My feeling is 10k beads (consistent Tconv-beads ratio) is the right way to go, but I also think 10k Treg would simply interfere physical interaction between beads and Tconv, potentially reducing Tconv proliferation regardless of actual suppressive activity of Treg.

Any experience, thoughts, suggestions are appreciated. Thanks!

Hey guys,

Forgive me if its a stupid question but immunology is unfortunately not my field of research (despite me finding it very interesting!) I was wondering if on top of a type 4 hypersensitivity to a certain substance a type 1 hypersensitivy can develop over time? If yes, is repeat exposure more likely to cause it? Would be very thankful for any ideas (including relevant literature suggestions) you might have!