TL;DR: ST2/IL-33 signaling could be a potential target of investigation in POIS.A follow up from this post:
https://poiscenter.com/forums/index.php?topic=3127.msg39195#msg39195https://poiscenter.com/forums/index.php?topic=2545.msg39495#msg39495==================================================================
Fidalgo's case report:
Immunophenotypical Characterization of a Brazilian POIS (Post-Orgasmic Illness Syndrome) Patient: Adding More Pieces to Puzzle"The majority of these cells are expressing CD38+, which suggests that the activation in this patient is more likely to happen via the CD38 molecule and there is no clinical explanation to that finding"
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Comparing total frequencies of leucocyte subsets in PBMC of POIS and the healthy individuals of the cohort, T cells and monocyte level were higher in POIS patient while B cell and NK cell levels were lower"
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The T cell activation profile comparison of POIS and controls (11 samples) shows that the frequency of CD4+CD38+ cells of the patient was higher"
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The plasma levels of soluble ST2 as a marker of gut mucosal damage in early HIV infection (there is an early phase and chronic phase, correlations between markers depend on phase)
"We observed correlations between sST2 levels and the percentage of CD4+ and CD8+ T cells expressing the immune activation markers (HLA-DR and CD38). Surprisingly, the correlation of sST2 was stronger with CD4+ than CD8+ T cells.""As the IL-33/ST2 is considered to be the guardian of the mucosal barrier..."
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sCD14, which is released from activated monocytes"
"We found a positive correlation between plasma sST2 levels and the Kyn/Trp ratio, which suggests that immune activation may be induced by metabolites generated either by gut microbes and/or by IFN-g following systemic viral infection"
"We subsequently assessed whether a correlation existed between sST2 and inflammatory markers IFN-g, TNF-a, IL-6, and IL-10 measured in plasma. A positive correlation was found for IFN-g only.In addition, IFN-g and IL-33 are known to counter regulate activation of ILC2s to control Tregs and type 2 responses, thus contributing to a shift toward Th1 response."
"During an acute infection, IL-33, an alarmin links inflammation, immune function, and tissue repair, whereas in the case of persistent infection, IL-33 may contribute to gut fibrosis "
"the alarmin response may wane over time because of tissue fibrosis."
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Fidalgo's NK cells are low which could make him susceptible to intracellular pathogens (virus). His elevated CD4+CD38+ levels could have a correlation with sST2 levels--->Infection could have happened at a mucosal surface like the gut. Recruited monocytes could raise the level of microbial translocation (sCD14). The combination of his other two conditions (two posts back) could indicate involvement of IL-33. IL-33 acts as an alarmin when barriers are "breached".
He had low levels of NK cells just like me. In addition to that, my elevated IFN-g could indicate activated anti-viral response. My elevated IL-8 level can indicate damaged epithelial or endothelial cells. IL-8 can be released by gut epithelial cells in response to bacterial translocation. The main source of IL-33 is the endothelial cell followed by epithelial cells. I wonder if the very high candida albicans LTT reflects CD4+CD38+ proliferation at a section of my gut, hence barrier penetration. In the article above it says that there is a positive correlation between ST2 and sCD40L (but only in the early phase). CD40 plays a role in IG class switching of B-cells. Could hyperexpression of CD40 be responsible for IgG4 class switching and could this be related to ST2?
POISers who recover over time may experience a transient decrease of "alarm sound". Yes the article is about HIV but who knows what other infection might mimmick this behaviour. Food for thought for sure.
Does the POIS response use IL-33/ST2 and/or CD38 signaling?
