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Faster Road To Inflammation

  March, 16 2004 9:14
your information resource in human molecular genetics
How do the joints of patients who suffer from rheumatoid arthritis become severely inflamed? An article in the April issue of Nature Immunology reports that cells from arthritic joints make more inflammatory factors because of their response to signals that are normally involved in cell death pathways.

Fas and its ligand, FasL, usually promote cell death. Richard Pope and colleagues show that macrophages can interact with each other via Fas and FasL. Macrophages are already known to trigger arthritic joint destruction through the secretion of proteins known as proinflammatory cytokines. Their new data begin to explain how the macrophage, a useful immune system cell, becomes part of the problem, rather than part of the solution.

When Fas and FasL interact, they release the intracellular signaling pathway of another set of surface molecules, namely interleukin 1 receptor and Toll-like receptor 4, from an inhibited state. Production of destructive cytokines then ensues. When the authors blocked Fas-FasL interactions, cytokine production dropped and the severity of arthritis in a mouse model was reduced. Because Fas and FasL are present on macrophages in conditions such as atherosclerosis, these findings may prove useful for understanding other chronic inflammatory diseases.

Author contact:

Richard M. Pope
Northwestern University
Chicago, IL
Tel: +1 312 908 9873
Email: rmp158@northwestern.edu

Also available online.

(C) Nature Immunology press release.

Message posted by: Trevor M. D'Souza

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