3 Kommentare
Avatar von User
Avatar von Wai Keat Ha

HI there! sorry for my disturbance. I read through your article but I can't the link between TRLs, T cell and B cell activation in autoantibody production... (I'm way too stupid)

Here's what I got from your article:

+ TLRs crosstalk with BCR siganlling

+ covid mRNA vaccination lower TLR4 and TLR7/8 siganlling -> TLR/BCR crosstalk disturbed? (due to TLR7/9 ratio altered) ->produce autoanbodies?

+ EF B activation (due to inhibition of TCR-mediated Tfh cell activation in CVID patients) is induced -> lacks TCR:MHC2 interaction (CTL can't kill autoreactive B cell; no maturation of b cell antibodies) -> atypical b cell (PC2) with high inflammatory profile produced? (life-long survival niche?) -> worsening humoral response (selective defeciency in either IgM or IgA)

+ useless antibody trigger HIV latency?

+B cell Pertubation as a hallmark in HIV infection (may be covid vaccination as well?)

would you mind to point out my mistake? Thx!

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Avatar von Genervter Bürger

So in the end: if the TLR-signaling is down it will alter the whole TCR/BCR-signaling. Messed up shit show

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Avatar von Genervter Bürger

TLRs are regulating via intra, inter - and extra cellular processes (cytokine signaling) T-Cells like CD4+ (maturated into Th, Treg and in this case important Tfh for example) which therefore regulate CD8+ and B-Cells. BCR is the activator of B-Cells and essential for the IGG-answer. At the same time, TLRs are also on and in the B-Cells reacting in a specific context dependent maner.

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