• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

T-Cell Sex diferences in IFN-γ and IL-17A Production

First of all I hope you are feeling better @Janet Dafoe (Rose49)

I also CC @Hip and @JaimeS

Ron and Mark Davis may find this interesting (the paper also talks about T-Cell expansion) :

Peroxisome proliferator-activated receptor (PPAR)α and -γ regulate IFNγ and IL-17A production by human T cells in a sex-specific way

Women develop certain autoimmune diseases more often than men. It has been hypothesized that this may relate to the development of more robust T-helper (Th)1 responses in women


Together, our observations indicate that human T cells exhibit a sex difference in the production of IFNγ and IL-17A that may be driven by expressions of PPARα and PPARγ.

and also

Collectively, these results suggest that two mechanisms are operating to regulate the sex differences in Th proliferation and cytokine production: (i) a mechanism that regulates the expansion of T cells that that is determined by the sex of the APCs and the T cell; and (ii) a mechanism that regulates Th cytokine production that is determined primarily by the sex of the CD4+ T cell. Herein, we focused on the T-cell-intrinsic mechanisms that regulate sex differences in the production of IFNγ and IL-17A.

As a reminder, Peroxisome Proliferators (PPARs) have been selected through Machine Learning Software which was used to identify potential biological targets relevant to ME/CFS (Nodes appear as "pparalpha", "ppargamma") :

Also the software was able to first identify the possible involvement of Pyruvate Dehydrogenase Complex, Fatty Acid and Bile Acid impaired Metabolism and -finally- a possible Liver pathology as suggested by Hanson et al .


Full text :