Effective Treatment For Rheumatoid Arthritis
Chronic inflammatory diseases, such as rheumatoid arthritis, involve autoimmune destruction of self-tissues by cells of the immune system that have somehow lost the ability to recognize friend from foe. Lymphocytes that make antibodies and those that trigger cell-mediated responses - B cells and T cells, respectively - contribute to this pathology. Any therapeutic strategies to treat patients with such diseases must therefore be able to inhibit activation of both cell types. The identification of such dual-purpose targets has been elusive. However, in the July issue of Nature Immunology (Vol. 2, No. 7, pages 632-637), researchers at Genentech in San Francisco have been able to inhibit B and T cells and halt disease in a mouse model of arthritis.
Immune cells respond to signals perceived in their environment by means of various receptors on their surface. Some signals promote cell activation, as required for battling infections, whereas others turn off this response. Ashkenazi and colleagues have focused on inhibiting interactions that activate lymphocytes, by confusing the system with “decoy” molecules. Specifically, they targeted the signaling molecule BLyS, which turns out to activate T cells, and not just B cells, through one of BLyS’s two or more receptors, TACI. Administration of soluble TACI blocked BLyS function and prevented the development of arthritis in mice. Thus, these signaling molecules are potential targets for developing new treatments for arthritis and other inflammatory diseases.
A News & Views (pages 577-578) on this article was written by Michael J. Lenardo of the National Institutes of Health, Bethesda, Maryland.
Dept of Molecular Oncology
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Michael J. Lenardo
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(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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