Jo was interested in CD24 because in repopulation following rituximab CD24 return behaved strangely. I think particularly in patients with thrombotic thrombocytopenia purpura. There aren't really any other B cell biologists working on ME/CFS as far as I know, now that Amok Bansal has largely retired from research. Even most other immunologists probably have little interest in CD24.
If B cells are relevant to ME/CFS I suspect the story is subtle and not a matter of some obscure specific autoantibody effect. Something that has proven important in lupus is the control of extra follicular B cell survival. It may also be relevant in RA in a different way. The question arises as to whether in ME/CFS the female predominance reflects a shift in maturation control for B cells, analogous to but not the same as in lupus, that allows for the formation of antibody populations that are not autoreactive but 'bad' for some other generic reason. If they were directed against foreign antigens and made by long lived plasma cells then rituximab would make no difference.
Maybe there is another 'quality control' mechanism for antibodies that is defective in people with ME/CFS such that they form antibodies to microbes that get in the way in some non-specific way - maybe by forming complexes of the wrong size or triggering too much ADCC or something. These antibodies might normally be selected against during an immune response through some interaction with CD57+ T cells outside follicles or something (just an illustration).
CD24 might be a marker of such a maturation shift, which might of course also be reflected in a shift in mean values for B cell metabolic pathways.
www.qeios.com
