Many proteins have homeostatic functions, according to the release, and this is the first study that indicates TNF may have some suppressive functions. In the study, researchers designed experiments stimulating macrophages with lipopolysaccharide, which stimulates receptors for inflammation. The researchers treated human monocytes and macrophanges with TNF and then changed these cells with LPS.
The TNF suppressed the inflammatory response of the macrophanges and monocytes. The protein GSK2 and gene TNFAIP3, which encodes the A20 protein, were involved in the inflammatory response to TNF. Patients who produce less A20 could be more susceptible to inflammation, thus rheumatoid arthritis.
“We think it is relevant to rheumatoid arthritis, not only because the cells we are studying (the macrophanges) are exactly the cells that migrate into the joints and make the inflammatory cytokines involved in rheumatoid arthritis, but because A20 is involved,” said Lionel Ivanshkiv, MD, associate chief science officer and physician in the Arthritis and Tissue Degeneration program at HSS, who led the study. “TNFAIP3 is one of the best linked genes in rheumatoid arthritis. There are polymorphisms in the A20 gene that have been linked to RA pathogenesis.”
Read the release about TNF for rheumatoid arthritis.
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