As a rule infection does not trigger autoimmunity. Almost everyone thinks it does but the evidence is strongly against, with the possible atypical exception of Gullain Barre syndrome. So a parallel with lupus does not fit here - one of the cornerstones of our Qeios piece arguments.
B cells with the wrong antibody gene rearrangements occur purely by chance but it would be possible for a variety of circumstances, including possibly infection, to facilitate the expansion of bad clones with plasma cell formation. It is hard to see how exertion would trigger this though. I think it is more likely that once the immune error has developed, then exertion triggers some short term signalling pathway that is sensitised in some way by the immunology.
Lupus is one of many autoantibody driven diseases. If ME/CFS involves autoantibodies then it fits in with all of them maybe. I initiated the use of B cell depleting treatment for lupus in 2000 with Maria Leandro and published the first study shortly after. Rituximab works very well but trials have been badly designed until recently. So we know that some of the autoantibodies come from short lived plasma cells in lupus but some hang around and come from long lived cells. That was the basis of Maria's PhD thesis.
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