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A key factor that controls the development of brain inflammation is reported in two studies in the September 2006 issue of Nature Immunology. Identification of this factor -- called interleukin 27 -- may provide a new target for treating inflammatory diseases of the central nervous system.
Nico Ghilardi and Christopher A. Hunter and colleagues studied two different mouse models of brain inflammation that resemble human diseases such as multiple sclerosis. Both groups show that brain inflammation is worse in mice that cannot respond to interleukin 27, a factor that communicates messages to immune cells. This more severe brain inflammation is associated with an influx of T cells that produce a molecule known to promote inflammation -- interleukin 17 -- into the brain. The treatment of T cells with interleukin 27 blocks the development of cells that produce interleukin 17. By preventing harmful interleukin 17-producing cells from developing, interleukin 27 could represent a potential therapeutic target for treating autoimmune diseases. Author contacts: Nico Ghilardi (Genentech, Inc., South San Francisco, CA, USA)
E-mail: ghilardi@gene.com Christopher A Hunter (University of Pennsylvania, Philadelphia, PA, USA)
E-mail: chunter@vet.upenn.edu Abstracts available online:
Article 1 (Ghilardi) Abstract.
Article 2 (Hunter) Abstract. (C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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