Jonathan Edwards
"Gibberish"
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@Jonathan Edwards
What would be your view on idea that pathogens might trigger autoimmunity by infecting important immune cells or important immune organs such as the thymus, spleen or bone marrow? If a chronic infection occurs in these cells or organs, it may conceivably create an environment which increases the chances of autoimmunity occurring, even if its actual occurrence is due to random factors in antibody production.
If we take enterovirus, this appears to profoundly affect dendritic cells:
Wild-type coxsackievirus infection dramatically alters the abundance, heterogeneity, and immunostimulatory capacity of conventional dendritic cells in vivo
Echovirus infection causes rapid loss-of-function and cell death in human dendritic cells
And coxsackievirus B4 seems to infect the thymus:
How Does Thymus Infection by Coxsackievirus Contribute to the Pathogenesis of Type 1 Diabetes?
And of course we know that Epstein-Barr chronically infects B cells.
I guess it is possible that infections might create local conditions that allowed an autoimmune process to get started when it would not otherwise but I am not quite sure how. EBV infection of B cells causes a permanent shift in B cell behaviour and this might be a permissive factor in a lot of adult autoimmune disease but it is a bit hard to tell since there is no way of studying an EBV uninfected population of any size. I am not sure that dendritic cells have much to do with autoimmunity. Autoantibody production probably makes use of antigen presentation by B cells themselves rather than other cells.
I have not read the hepatitis C paper but the quote looks dubious to me. One thing we are pretty sure about now is that TH17 cells are not important in RA - and I rather doubt they are important in any of the autoimmune diseases mentioned. They seem to be important in seronegative spondarthropathies instead.