Ethanol consumption inhibits T<sub>FH</sub> cell responses and the development of autoimmune arthritis.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 32332730.
- Also identified by DOI 10.1038/s41467-020-15855-z and PMC identifier 7181688.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Alcohol consumption is a consistent protective factor for the development of autoimmune diseases such as rheumatoid arthritis (RA). The underlying mechanism for this tolerance-inducing effect of alcohol, however, is unknown. Here we show that alcohol and its metabolite acetate alter the functional state of T follicular helper (T<sub>FH</sub>) cells in vitro and in vivo, thereby exerting immune regulatory and tolerance-inducing properties. Alcohol-exposed mice have reduced Bcl6 and PD-1 expression as well as IL-21 production by T<sub>FH</sub> cells, preventing proper spatial organization of T<sub>FH</sub> cells to form T<sub>FH</sub>:B cell conjugates in germinal centers. This effect is associated with impaired autoantibody formation, and mitigates experimental autoimmune arthritis. By contrast, T cell independent immune responses and passive models of arthritis are not affected by alcohol exposure. These data clarify the immune regulatory and tolerance-inducing effect of alcohol consumption.
Medical subject headings
- Alcohol Drinking
- Arthritis, Experimental
- Arthritis, Rheumatoid
- Ethanol
- T-Lymphocytes, Helper-Inducer