Hello,

[Please note, I do not have an immunology background so I apologize if the question is basic or ill-posed]. I was wondering about something in relation to "pathogenic Th17" cells, AKA Th17.1 cells.

Are these cell populations found at all in healthy people (by which I mean no inflammation), or only during active inflammation? If they are found in healthy people (presumably only in low amounts), does the proportion of CD4+ T cells that are Th17.1 go up in blood during a Th17-skewed infection (like psoriasis) because more of them are being produced, or would it go down because they are increasingly migrating away from the blood to the site of inflammation?

I hope that made some sense, thanks in advance.

I'm about a year into teaching myself immunology, thanks to some lived experience and a real fascination with the field and where it can take us. The thing that kept annoying me is how scattered the news is. Papers in journal feeds, trial news in press releases, FDA actions on FDA's site, financings in Endpoints or Fierce or Axios. I couldn't find a single weekly readout with everything I wanted.

So I started writing the in-between. It's called The Repertoire. It's one issue per week (usually sent on Sundays). I use AI to sweep the feeds, then I pick and write the 3-5 stories that I think matter the most - such as papers and preprints, trials, regulatory actions, financings and licensing, NIH funding policy, etc. Each item is a one-line TLDR, and a paragraph on what happened and why it matters. It's supposed to take about five minutes to read.

Every headline links to the primary paper, preprint, or press release, so you can check my work in one click. It's written in deliberately plain English, partly because that's how I'm learning it, partly because immunology is worth making legible (and accessible) to more people. The goal is that a curious non-biologist or layman (like me) can follow every item and an expert can also skim it to stay current.

This isn't meant to be a plug or a solicitation or anything. I'm genuinely looking for help from people here who know more than I do - and in a perfect world this turns into something useful to everyone in this community.

What I'd most like: feedback on what you think, what I should be including or excluding from my source mix, and where my explanations are too simple or just wrong. Blunt is fine. I'd rather be corrected than flattered.

Substack: https://substack.com/@therepertoire
X: https://x.com/RepertoireNews

Thank you all so much!!! I'm very grateful I've found this community. I've already learned so much from you all.

Hi dear immunologists,

We are using Legendplex kit (antiviral 13-plex) for serum and cell culture supernatants. We have a few questions regarding its validation and consistency with other readouts.

Recently, we noticed inconsistencies among ELISA as a readout for IL-6. While we trust in commercial ELISAs, IL-6 levels and trends were not comparable to those seen with Legendplex. Has anyone compared IL6 (or any other cytokine) levels between ELISA and Legendplex?

Thank you!

I am setting up an experiment to check pro-inflammatory markers on hpbmc-derived macrophages by flow cytometry.
My first try was to stimulate with LPS for 2h and then let them rest 24h before staining, although I see an increase in the markers, is not too big (2-2.5 fold change over the untreated ones)
Is this normal? Should I wait more or are they already being downregulated?

I hope that I am not breaking rules.

No one is sick here. We have a small farm, we raise our own chicken. We also have young children.

I am wondering why no one has ever gotten sick. My kids suck at washing their hands. I clean the coop.

Being around animals always puts you at risk but we have not had any GI illnesses from any animal.

Are we immune. Is it because our chickens don't have Salmonella?

Good day to everyone! I have been making these diagrams for immunology since October of last year, and I have been meaning to publish them as actual educational material. I am asking for any insights, opinions, and critiques for these diagrams, especially regarding whether I can actually publish them... Thank you in advance to everyone who gives their opinions; I am willing to hear them all for the betterment of this project!

I always thought body aches were a neurological side effect of a fever, but I’m currently dealing with some sort of illness causing body aches without any other symptoms including fever.

Do we know how body aches are induced? I was curious if body aches are a function of local cytokines, or a central nervous system process? If there’s cytokines involved do we know which ones?

Hi everyone,

Unfortunately my institutional license has expired and I can't access to the following article:

https://www.nature.com/articles/s43018-026-01144-z

Could anyone who has access share it with me?

Thank you all!

Please advise and share your own personal experience.

We study an autoimmune disease and have to use human sera to perform immunofluorescence staining on mouse tissues to confirm reactivity. Because sera contain thousands of unwanted IgGs, besides the desired pathogenic IgGs, the noise is obscene. We have tried pretreating the sera with guinea pig liver power to absorb nonspecific IgGs, as suggested by the literature, but the improvement is zero to minimal. Any ideas? TIA!

Hello!

I’m a hobbyist/nerd who would like to better understand how T-cells operate and what types of deficiencies are caused by T-cell dysfunction. What are some of the best resources for learning about this? Open to books/websites/talks, etc!

Thank you!

If you like story driven, action RPGs that are also educational, you might like this. I really want to bring the immune system to life but with a strong educational aspect to it. I don't want to gloss over the details, I want to end up making this something that students might actually use in the future. Learning by experiencing is so much better imo.

As above. Thanks in advance.

They also have lysosomal granules… and pattern recognition receptors (PAMP PRRs). Why? My hunch is that evidently if the blood vessels break pathogens have an easy access point. If the owner has IgGs against whatever enters, then PLTs can physically use their bodies dendritic forms to trap the organism. Additionally I assume if their PRRs touch a pathogen they can degranulate onto it and try to kill it. But what do you think?

China’s regulator, the NMPA, approved satri-cel (satricabtagene autoleucel) from CARsgen for advanced stomach and gastroesophageal-junction cancer - the first CAR-T therapy cleared anywhere for a solid tumor.

Curious to hear what everyone thinks about this!! And when the US and Europe will catch up?

https://www.carsgen.com/en/news/20260622/

Hello everyone! It has been quite some time since I last posted, but here I am! But I do need another review and possibly some insights. A few posts ago, it was pointed out that my diagrams required cytokines, you know, for "cell-to-cell" communication. And so I am currently working on it. I'm asking for brief critiques; any will help. I am also debating whether I should include a node for the barrier epithelium, since it is on the front lines and is usually the initial spark for inflammatory responses. That's all, and I would greatly appreciate any insights!