ME and inflammatory bowel diseases

When I saw this I thought that if autoantibodies are the cause of 'long Covid' then 'long Covid' and ME/CFS couldn't be the same since the Rituximab trial was negative. Then I wondered about chronic ulcerative colitis, both because I was diagnosed with it (though it "vanished" after a month on sulfasalazine) and my mother had also been diagnosed with it (she died of bile duct cancer, a known sequela to chronic ulcerative colitis). I googled "autoimmunity in chronic ulcerative colitis" and found this 2017 paper:

Efficient long-term depletion of CD20 + B cells by rituximab does not affect gut-resident plasma cells

This was an attempt to see if B-cell depletion could cure inflammatory bowel diseases like Chron's disease and chronic ulcerative colitis. It did not. The authors suggest that the reason for the negative effect was because "rituximab did not deplete colon-resident plasma cells (PCs) while ablating all CD20+ B cells in tissues and in the circulation."

I've wondered if inflammation of the GI tract could somehow be a factor in ME/CFS, mainly because I developed IBS symptoms a few months following onset. These persisted until they became IBD symptoms some years later. As I mentioned, they resolved after a month on sulfasalazine. The doctor thought I'd been misdiagnosed with chronic ulcerative colitis and had simply recently acquired a transient case of "Montezuma's Revenge." Arguing against this was the fact that I had never been out of the country and that my "transient" case had been going on for several years.

The abstract also says:

So, if gut inflammation is somehow tied into ME/CFS, might this explain why patients didn't show improvement in the rituximab trial - because their intestinal-resident PCs were spared depletion?


I realize I'm in over my head here and speculating way above my pay grade based on one paper's abstract .

 

Ulcerative colitis is not generally regarded as a true autoimmune condition, although the majority of physicians know so little immunology they would not notice. UC and Crohn's have pathology indicative of T cell misbehaviour and have genetic cross-associations with the T cell based spondarthropathies. (In spondarthropathy there inso evidence that the T cells are 'autoimmune', just inappropriately active.) Autoantibodies do occur in a small proportion of inflammatory bowel disease patients but there is not much to indicate they are important. When we started using rituximab we made a very clear prediction that it would not be much use for Crohn's and UC and might well make them worse.

The persistence of gut plasma cells seems irrelevant since plasma cells persist mostly after rituximab anyway. If antibodies are relevant to Crohn's and UC there inso particular reason to think they are made in the gut. The gut is normally full of plasma cells - shedloads of them.