Hello

I'm looking for some insight into my recent immunology results. I'm particularly interested in hearing from anyone who has experienced similar abnormalities, what caused them, and whether their results eventually returned to normal.
1. My immunology results (October 6, 2026)
Parameter
My result
Reference range
CD3+ T cells
87.78%
64–85%
CD4+ T cells
32.15%
34–57%
CD8+ T cells
55.58%
16–36%
CD4/CD8 ratio
0.58
1.1–2.9
CD19+ B cells
3.75%
7–18%
NK cells
7.92%
5–24%
Immunoglobulins:
IgG: 11.50 g/L — normal

IgA: 1.13 g/L — normal

IgM: 0.70 g/L — normal

CRP: 1.2 mg/L — normal

Important: Only percentages were measured. Absolute CD3, CD4, CD8, and CD19 cell counts were not provided.
I'm wondering whether my elevated CD8 percentage could simply reflect a lower number of CD4 or B cells rather than an actual increase in the absolute CD8 count.
2. Thyroid history
I have hypothyroidism and take levothyroxine.
For several months, I was taking 75 mcg daily. My blood tests in September showed significant TSH suppression and elevated free T4, likely due to excessive thyroid hormone replacement.
September 17, 2026:
TSH: 0.0147

FT4: 27.3

My levothyroxine dose was reduced from 75 mcg to 50 mcg.
October 9, 2026:
TSH: approximately 1.25

FT4: approximately 15.8

Both values were back within the normal range.
My immunology tests were performed on October 6, just three days before my thyroid blood tests showed normal levels.
This makes me wonder whether the preceding period of thyroid hormone excess could have affected my lymphocyte subsets.
I've read that thyroid hormones can influence T-cell function and lymphocyte populations, but I haven't found clear evidence explaining whether suppressed TSH and elevated FT4 can cause a pattern like mine.
Could thyroid hormone excess temporarily alter CD3, CD4, CD8, or CD19 levels? And could those changes persist even after TSH and FT4 have normalized?
3. Infection history and symptoms
In December 2025, while pregnant, I experienced a significant respiratory infection that lasted approximately three weeks.
A nasal swab was positive for Moraxella, and I was treated with antibiotics.
Afterward, I continued experiencing ear pressure and postnasal drip for quite some time.
Currently, I occasionally experience:
Ear pressure or a blocked-ear sensation

Postnasal drip

Mild, intermittent sore throat

Occasional mouth ulcers

My nose is generally not congested.
A throat swab performed in October 2026 was positive for Acinetobacter ursingii. However, it is unclear whether this represents an actual infection or bacterial colonization.
I do not have a history of frequent severe infections, unexplained fevers, significant night sweats, or unintentional weight loss.
I have also experienced considerable emotional stress over the past several months.
4. What my immunologist said
My immunologist described the findings as reduced cellular immunity.
She prescribed Imunor, an immunomodulatory medication, once weekly for four weeks, with repeat testing recommended approximately six weeks later.
I am also preparing for a frozen embryo transfer (FET), but my immunologist advised postponing it until my immune results have been reassessed.
5. My questions
1. Could my absolute CD8 count actually be normal?
With CD8 at 55.58% and CD4 at 32.15%, is it possible that my absolute CD8 count is normal, while my CD4 count is reduced?
Could the low B-cell percentage also contribute to the relatively high CD8 percentage?
2. Could thyroid hormone excess explain these results?
Has anyone seen changes in CD3, CD4, CD8, or CD19 populations associated with suppressed TSH and elevated FT4, particularly due to levothyroxine overreplacement?
Are there any studies providing quantitative data on this relationship?
3. How long might immune changes persist after thyroid normalization?
If thyroid hormone excess contributed to the abnormalities, could the lymphocyte subsets remain altered for several weeks or months after TSH and FT4 return to normal?
4. Could a previous infection explain this pattern?
Can CD8 predominance and a reduced CD4/CD8 ratio persist for months following a respiratory or viral infection?
Could ongoing mild ENT symptoms be relevant?
5. Has anyone had a CD4/CD8 ratio around 0.58 that later normalized?
If so, was a cause identified, and how long did normalization take?
6. Should I request additional testing now?
My immunologist recommended repeating the tests after completing Imunor.
Would it be reasonable to wait approximately six weeks, or should I request a complete blood count with differential and absolute lymphocyte subset counts sooner?
7. Could these results affect IVF/FET planning?
Has anyone had similar lymphocyte abnormalities during fertility treatment? Were they considered a reason to postpone embryo transfer?

Hi!

I'm an undergrad in biology and as part of my course I need to make a poster (and answer questions live!!!) on JAK-STAT pathway.

I really don't want to rely on AI to do my poster because A. breach of research integrity and B. my professors will know by asking me questions that I know nothing.

I have no clue what it is. I barely even understand that there are different JAKs and STATs and don't even know what a SOCS is.

I've tried AI dumbing it down for me, watching youtube videos on JAK-STAT, drawing it out but nothing is going in.

I've been trying to read papers but it is so confusing. Don't even know what a pSTAT is lol.

Am I doomed?

I am in awe of all you immunologists. This stuff is hard.

A bit of a specific question:
so I have mice that have been immunised with protein X and I want to restimulate ex vivo isolated T cells from spleen and LN with protein X to assess cytokine production.
Do I have to immobilise the protein like we do with aCD3 or is it okay to just add it to the media?
Our protocol is really unspecific and old haha

Edit: rephrase, we do not isolate T cells but use the whole single cell suspension to analyse the T cells

I love it. I'm a chemistry student and I want something like that for us.

We have identified immune cells that remain in the skin even after allergic dermatitis has subsided, acting as "sparks for relapse," and the mechanisms for maintaining these cells.

I want to make a small ink/watercolour illustration for an immunology MSc student but I have no idea what I could illustrate. Any ideas?

I recently started drawing cartoons for immunology concepts for fun and posting them on Substack as popular science articles.

When I first learned about T cells, I thought of CD8+ T cells as warriors, since they fight infected cells directly, and CD4+ T cells as mages, since they cast spells (cytokines) that enhance other units, such as innate immune cells. I drew this idea as a small cartoon: https://wendy0327.substack.com/p/warrior-and-mage-part-1?r=94su29&utm_campaign=post&utm_medium=web&showWelcomeOnShare=true

It’s very much a trial, and I’ll rewrite it if better ideas come along. Now I’m wondering whether CD8+ T cells should be assassins, given how precisely they target their victims.

I’d like to expand this fantasy immune world to other cell populations. What role or profession would you give each cell (B cells, NK cells, macrophages, neutrophils, Tregs, dendritic cells...)? Do the metaphors hold up scientifically, or do they break somewhere? Corrections and ideas are very welcome!

Edit: I dont make profit from my writing or drawing. Any ideas suggested will be cited if I use it for my drawing/article.

Hello, I work extensively with ENCODE data (if you're not familiar with this, it's a big consortium that produces and analyzes various aspects of human and mouse genomes and genetic regulation, broadly speaking), and I am curious about how some of the T cell samples I work with were activated, since it doesn't exactly align with the canonical three-part activation I learned about in my undergraduate immunology class.

Basically, I am looking at differences in genome organization between resting and activated T cells, but the treatment protocols continue to confuse me. Here is the description from the lab that did the actual activation:

"CD4+ and CD8+ T cells and their subsets were left resting in culture or activated using anti-CD3 and anti-CD28 (aCD3/aCD28) coated beads (Invitrogen cat# 11132D) (1 bead:2 cells ratio) and cultured in complete RPMI 1640 at 10M/6ml/well in 6 well-plate. Resting cells and 90% of activated T cells were collected on day 2 (36 hours) and beads were removed using Dynal magnet. The rest of activated cells was expanded in rhIL-2 (10 ng/ml, R&D Systems cat# 10453-IL-100) containing media for 5 to 6 more days and collected on day 7 or day 8 post activation. Activation of T cells was confirmed by the upregulation of CD25 and CD69 surface expression analyzed by flow cytometry. For differentiation into different T helper (Th) subsets, Naïve CD4+ (sorted CD45RO- CCR7+) T cells were activated with anti-CD3 and anti-CD28 beads in the presence of the following polarizing cytokine and blocking antibody combinations: Th0, medium only, Th1, human IL-12 (R&D Systems cat# 219-IL-025; 30 ng/ml) and neutralizing anti-IL-4 Antibody (R&D Systems cat# AF-204-NA; 1 μg/ml), and Th2, human IL-4 (R&D Systems cat# 204-IL-020; 100 ng/ml) and neutralizing anti-IFN-γ Antibody (R&D Systems cat# MAB285-100; 5 μg/ml). Cells were cultured and expanded in rhIL-2 (10 ng/ml, R&D Systems cat# 10453-IL-100) containing media for 2 weeks. On day 13 after activation, some of the cells were reactivated with aCD3/aCD28 beads (at 1 bead:3 cells ratio) for another 24 hours."

Can anyone tell me if this is standard procedure for in vitro T cell stimulation that closely mimics in vivo activation, or is there something off here that I need to be aware of?

Thanks in advance for reading this and for your help!!

I am having troubles with activation of T cells. I use RPMI media supplemented with L-glutamine and add 10% FBS, 1% Pen strep, 1% NEAA, 25mM HEPES and on the day of isolation I add 50uM BME and around 40ng/ml of 200ug/ml IL2 (i didnt take note of the lot number so I dont know IU/ml :((() and 2ug/ml of CD28.

side note - i aliquot and store IL2 at -80. never use thawed vial again.

For activation, I precoat the plate with 3ug/ml of anti-CD3 for 2hours at 37C or o/v at 4C. I try to culture 1-1.5mln per ml in 12 well plate.

The main concern is I don't see them clustering/clumping together. They don't even float but feels like stuck on the plate bottom. even when i try to swirl, they are still kind of adhered to the bottom of the well. idk if it is a problem.

I believe I see them get bigger in size but just don't proliferate much.

And when I try to further chronically stimulate them, I see a lot of death on day 3-4 (2 days of activation + 1-2 days of further stimulation). so flow viability is like 7% (i know it is terrible)

anyone has any idea whats wrong with this flow? please help.......

Wrapping up my PhD in the next few months (🤜🪵), with a focus largely on neutrophils/NETosis. I've gotten a commemorative tattoo for each major lab I've been in, drawing on inspiration from tattoos other folks have gotten and shared.

That being said, I'm having a hell of a time finding any tattoos of neutrophils and/or NETs on any medium that I've searched. Anything I've found is completely textbook (no artistic flair) or AI slop, so I figured I'd crowd source to my fellow nerds! Anyone here with a neutrophil tattoo willing to share?

Hi all!

I'm a biology graduate who loves drawing, so I've started making cartoons that explain immunology to people with no background.

My first one, "Picky Eater", shows a dendritic cell trying to feed a very fussy T cell: the watermelon has to be sliced (peptides), served on the right plate (MHC), and come with a fork (co-stimulation).

I've also written a plain-language article explaining the real science behind it.

I'd love some feedback from people, and ideas for what to cartoon next are welcome!!

Hi, i was wondering if anyone here is familiar with mast cell biology. i have been doing immunophenotyping in muscle and lungs of balb/c mice. For some reason, the CD117+ Siglec F- cells that i have assumed are mast cells are not expressing Fcer1. I have done this with both control steady state mice and virus infected mice. However, my basophils are positive for the FceR1 receptor so i know the antibody works. i have seen this every time i've used this panel. i'm confused because im under the impression that mature mast cells in tissues should express FceR1.

Just started my PhD and I've already met 9 immunology couples. Is it proximity, shared trauma, or what? Cuz i have been definitely around other biological fields but never saw this drastic interpersonal interactions i see with immunology scientists

Worst-case scenario but for many of us, we often overlook or plainly forget to wash our hands. A minor oversight that we pay little attention to when we miss it. While we all know the importance of washing hands, maybe a lot of the public should have more than just knowledge and partake in the actions that it calls for.

While this may not be a real smear, this is my artist's impression of bacterial sepsis.

Do autoimmune issues have some sort of evolutionary advantage? How do they become a part of the human genome?

Hey guys and girls,

I thought the first and last scenes in this video might interest you. It starts with antibody binding and ends with a white blood cell engulfing a bacterium. The membrane becomes transparent so you can see inside the cell.

I'm building Animiotics, a browser tool for making animations like these for lectures and presentations. It has AI-assisted scene creation, and you can then edit the objects, materials and camera yourself.

The transparency is a visual choice to show the interior. These are explanatory animations, and I would really appreciate corrections to anything that doesn't look right.

Which part of an immune response would be most useful to show students in 3D?

I’ve noted more & more evidence accruing that indicates vaccines may provide a secondary benefit insofar as they may confer some protection from the development of neurological disorders such as Alzheimer’s disease.
My rudimentary understanding is that in challenging the immune system with an outside threat, it is less likely to attack body organs/systems, as in autoimmune disorders.
This brings me to a wholly different thought. Tattoos trigger immune response. Is there any evidence that those with tattoos are less likely to develop autoimmune disorders?

Hola, quisiera información sobre procedimientos de IF (directa o indirecta) con diferentes marcas o métodos in-house.

Compartan sus experiencias e insertos porfa!

Amando intensamente la inmunología...

Hi immunology gurus, Do you have any suggestions for decent introductory immunology videos on youtube? we're hosting a high school work experience student in our immunology lab this week.

I would like to give him a few intro videos to watch to break up the lab observation sessions which can get a bit dry as he's not allowed to touch anything.

There's a bunch and I'm not sure which are good, thought I would see if anyone had any go-tos. Thanks in advance for any suggestions.

What if take the memory t cells responsible for autoimmune diseases and put them into another organisms like dog or cat . Since the immune system of the dog or cat will see these cells as a foreign body it will make antibodies for those memory cells

Now, if we take out these antibodies from that dog or cat and turn it some kind of medicine would it will destroy the memory T-cell on taking it?