Our Prof told us, that autoimmune diseases are often triggered by infections, psychological traumatic events, chronic stress or surgeries. Basically by anything, which stresses the immune system to a large enough amount. He mentioned, that the malfunctioning T and B cells are already there, but a random stressful event and the following immune and cytokine turmoil activates them. Is that just an nice theory, or do we have actual empirical data for this claim?
Basically, immunologists are intellectually lazy and they are sheep. The idea that autoimmune disease was triggered by infection started up in the 1960s, simply because of rheumatic fever, which is not an autoimmune disease but is triggered by an infection. It looks enough like rheumatoid arthritis for RA to be named -oid after it - but that is simply because both involve immune complexes. And it is because RA looked a bit like rheumatic fever that a lot of infectious disease specialists became rheumatologists when they were out of a job when penicillin came along in 1946.
When it became clear that a genetic component was likely the immunology sheep all had slides made up that looked like the slides the other sheep put up saying disease was caused by genetics and environment. That way everyone knew they were really cool flock members with white hot ideas.
Except for a black sheep called Paul Stastny, who actually discovered what the main genetic link was - the 'B cell antigen Dw4' (now known as HLA DR4). Pal had a quiet, sensible way of lecturing and always pointed out that apart from the genetic factor the rest of the causation looked random (stochastic). He was well enough read to know that in epidemiology stochastic components are an essential part of the model. Nobody listened.
So it sounds as if your Prof was one of the usual white sheep. The molecular mimicry theory was designed to explain rheumatic fever but it does not even do that -nobody ever found the mimic antigen.
Years later it was discovered that smoking lowers your threshold to get RA. We still do not know why but it may have to do with citrullination of proteins in damaged lung. It may not. But infection and trauma and psychological stress - as far as I know the evidence is 95% weighted against any relevance for those for most autoimmune diseases. You get sheep in Australia I am told!
If you eradicate almost any B cells, why isn't the body prone to more nasty opportunistic infections? I know, B cells aren't the only defence of the body, but shouldn't the loss of B cells be a larger problem for the immune system? The good plasma cells tend to live longer and continue to produce antibodies against old pathogens, right? But what about new pathogens? With no B cells, new plasma cells cannot develop against new pathogens and new antibodies cannot tag them. So is the rest of the immune defence enough to keep them in check?
B cells are actually a fat lot of use if you meet a new infection. It takes about 21 days to develop a full IgG response to a new antigen. Most infections kill you long before that - maybe in a week or so. So the function of antibody is really to stop you having to fight off a second dose - to nip it in the bud with memory antibody - and perhaps most important of all to provide newborn babies with something to keep them alive when they first come in to the world and start meeting germs all over the floor.
There is no doubt that there is something surprising about the fact that rituximab helps autoimmune disease without causing hardly any problems for most people. As Martin Glennie said when he introduced me at a conference 'Jo's treatment idea was nuts but it seems it turned out to be right'. It looks as if it relates to plasma cell half life as you say.
I did tell patients on the early rituximab studies not to travel to Sharm El Sheik or Mobutu if they could help it while having rituximab but in fact tropical diseases are even less antibody dependent than the usual ones and I have not heard of any problems with travel since.
B cells are really trainee cells. You can be without them for m onths. And they were never a front line army.
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