In the December 1 issue of the Journal of Clinical Investigation, Yoichiro Iwakura and colleagues from the University of Tokyo studied the role of T cells in the development of autoimmune arthritis in mice lacking IL-1Ra. The authors demonstrated that mice deficient in both T cells and IL-1Ra did not develop arthritis. Arthritis development also appeared to be markedly decreased in cases of TNF-alpha deficiency. The authors found that IL-1Ra produced by these T cells act on the T cells themselves to induce TNF-alpha expression and TNF-alpha in turn induces OX40 expression on T cells. As inhibition of TNF-a or OX40, the latter being an activation antigen on T cells, which invade tissues and cause autoimmune destruction was effective in suppressing the development of arthritis, the authors suggest that their study may provide a clue for the development of new therapies for RA.
TITLE: TNF-alpha is crucial for the development of autoimmune arthritis in IL-1 receptor antagonistdeficient mice
Center for Experimental Medicine
University of Tokyo
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Contact: Brooke Grindlinger
Journal of Clinical Investigation