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!

Tell me why my reasoning is flawed. Most immunology knowledge has already been discovered. What’s the point in further research? I could definitely be wrong. Tell me why I am wrong.

Hey there. I’m trying to induce T-reg cells from PBMCs but I haven’t been able to find them (I’m looking for FOXP3+ cells). Does anyone here has a protocol for stimulating them? I’ve tried with PMA/Ionomycin and IL-2. Note: I know the fixing/permeabilization procedure is not the problem since my controls are okay

I realize this is a wildly oversimplified way to think about this, but I think it's a fair question. I'm currently taking an immuno course and this question came up.

If DAMPS activate local sentinel cells and initiate the innate response in tissues , couldn't we just formulate a cream with DAMPS to boost wound healing? I know there are creams that stimulate anti-viral responses, e.g. imiquimod, but what about for general wound healing, like a scrape or a cut?

When a phagocytic immune cell consumes a bacterium and breaks it down with digestive enzymes, what are the usual chemical products of this? Also, how much of this is re-used by the body?

Hi everyone,

I am distinguishing neutrophils, monocytes, and lymphocytes using one color (FITC) on the LSRFortessa, with optimized voltages (FSC: 230, SSC: 300). Due to limited access, I've switched to the FACSymphony but am struggling to replicate the voltages. Image 1 shows the Fortessa results, and Image 2 is from the FACSymphony.

Image 1

Image 2

I’m analyzing some LCMS-MS proteomics data from primate serum. The initial analyses was done in Spectronaut, and downstream analyses were in R. Primate FASTA was used and there was no mapping to a human ortholog. These animals were healthy controls.

At both the peptide and protein intensity level reports I’m not seeing any specific IgG, but do see IgM and IgE. Any reason why this would be that I should investigate or something I’m just totally missing?

I’ll also add that serum albumin, A-1, and C3 were all detectable. Albumin was the most abundant protein (expected).

Hi,

I had completed my MsC Immunology & Immunotherapy last year. But I’m not able to find good opportunities cause I am a fresher. How to apply for Job or what should I keep in my mind before applying. Is there any internship opportunities that is available? I reside in Uk currently and it’s really hard to get opportunities as all need experience. I need some help & suggestions.

Hi!

I work at a diagnostic pathology lab as a immuno-technician in the Netherlands. Regularly, I have to setup new IHC stains. I am looking for a place where I can ask questions to IHC experts. I thought there would be a place somewhere on the internet where a forum exists on that subject but i can't find one! I think that is quite strange. Does anybody here know of a forum or something? I know the NordiQC website but they only have information on regular antibodies, not the new exotic antibodies. And they don't have a forum.

Would anyone have any research as to the cause of allergies and the bodies response to it? Why it happens. What could be causing them.

For a paper I'm currently writing, I cultured splenic FO B cells (separated via MACS) in RPMI 1640 medium containing 25 mM HEPES, containing 10% fetal calf serum, 2% L-glutamine, 100 u/mL mix of penicillin-streptomycin, 1% sodium pyruvate, 1% non-essential amino acids, and 50 μM β-mercaptoethanol. We cultured these cells for three days at 37 degrees Celsius and 5% CO2, seeded at a density of 200 000 cells per 200 microliters. However, after these three days, we found that only around 30% of our cells are currently alive.

I was wondering if we made a mistake in our protocol. Does anyone have experience with culturing B cells, and is it normal for FO B cells to die off so quickly? I can imagine that it might, as the cells could die because of a lack of stimulation, any tips?

Hello, I'd like to familiarise myself with lab techniques used in immunology labs. We recently did ELISA and although I've done enzyme assays in biochem labs I realised I didn't completely understand the logic behind the maths etc (I'm not very good at maths to begin with) and want to really learn at a higher level. If you have any textbook or review article recommendations or even a list of techniques that are good to know, please share them.

I am a 29 year old nurse manager from South Australia and I am beginning to realise that I am really passionate about cancer biology and immunotherapy. I have decided to spend 2025 volunteering in a laboratory to gain some wet lab experience to prepare myself before I enrol in a research degree (ideally 2026). On top of this, I also want to learn as much as possible about cellular and molecular inflammatory patterns since the biology that I studied from my bachelors was very rudimentary. The internet is an awesome place to learn but as much as I love wikipedia, I’m finding it hard to focus on a topic because of all the links that take me to a different page whenever I encounter an unknown/unfamiliar term. Do you have any suggestions on what free courses might be available out there? I appreciate your time and consideration.

Measles infection can remove some memory from our T and B cells. Does it have an effect on IGE antibodies?

My shower thought of the day is if someone had a severe food allergy could the sensitization be undone by a measles infection?

I am currently deep in writing of my Honours thesis and am trying to come up with some justification for what happened in my experiments

My project involved generating NK cells from human PBMCs using a modified K562 cell line. I confirmed the majority of cells present were NKs using flow cytometry.

I have a line of MCF-7 breast cancer cells that have been transfected and express HLA-E loaded with the HLA-G derived peptide (VMAPRTLFL) and compared NK cell killing against a control group of MCF-7s with no HLA-E expression. My problem is that every article I have read (a lot at this point) is telling me that the HLA-E should inhibit NK cell lysis by a noticeable amount, yet my cytotoxicity assay saw that both cell lines had the exact same, high lysis activity up to 90% at the highest concentration of NKs

Im really hoping there is an HLA-E expert somewhere in here because I am stumped and frantically searching for some justification of this is not going well

So I have a lecture on Antigens for the medical students and this is kinda my first time presenting a lecture like this and I don't know what to do? Which resources to use? How to explain it in the best way possible?

I'm 34 weeks pregnant and this weekend I had an awful stomach bug. Thankfully I'm through the worst of it, have the care and medicine I need and don't require medical advice.

This stomach bug, Norovirus, is a rapidly mutating virus. I can't seem to find a straight answer on-line. Am I producing antibodies against this particular strain and if so, is any of it get past placenta to them and giving them any immune benefit?

Hi immunology folk,

I'm the parent to an immunocompromised child aged 3 that has SAD (pneumococcal and strep) and IGG Sub 2 deficiency. I've just recently started a new job as a tech assistant in microbiology my main role at this time is culture set up for swabs. My question is, am I endangering my child by being in this role? I'm literally in contact with gram positive bacteria daily, and I hadn't thought of the risks until now (2weeks into the new role) and wondering if maybe I should reconsider my work choice. Child is on prophylactic antibiotics.

Thanks in advance for your time!

Hi! Can you recomend me books, chapters or papers to learn about neuroinmunology?

I'd appreciate an intuitive yet comprehensive breakdown to understand it thoroughly to do well in exam and later in clinical setting. How should I approach/what should I look out for/how can it be broken down and understood ?

Thank you

I know that I have a VERY basic understanding of the immune system, so please don't attack my stupidity ...

I understand that killer T cells kill self-cells that display viral proteins on MHC-I, and that natural killer cells kill cells that don't have MHC-I, and that these are mostly effective at killing virus-infected or cancer cells.

But we know that there are various kinds of bacteria that can become intracellular, and presumably being inside a cell is a relatively safe place for bacteria to replicate and take up resources. What does the immune system do about intracellular bacteria?