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COVER PICTURE: Inflammatory arthritis is associated with the release of a network of cytokines, including interleukin (IL)-1. Mice that are IL-1 receptor deficient are protected against developing joint inflammation and destruction in an immune complex model of arthritis (top). The administration of a Toll-like receptor-4 ligand, lipopolysaccharide, concomitant with arthritogenic serum in IL-1 receptor-deficient mice, however, resulted in acute synovitis and bone erosion (bottom), suggesting that innate immune mechanisms may perpetuate inflammation and bypass the need for IL-1 in chronic joint inflammation. See related article by Choe et al.,
(pages 537-542).
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