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We all know someone who is allergic to nuts, pollen or penicillin. Or worse still, an unfortunate person allergic to chocolate or strawberries. The familiar signs of allergy, an immune response to an innocuous substance, include hay fever-like symptoms, irritation, hives, fluid retention, increased mucus production, constriction of airways and even anaphylactic shock. In the March issue of Nature Immunology (Vol. 2, No. 3), Steinman and colleagues from Stanford, USA, and Milan, Italy, show that a fragment of one of our own proteins, a self-antigen, can induce the worst symptom of allergy, fatal anaphylaxis.
The researchers used a mouse system that models the human disease multiple sclerosis. They found that if they re-injected a self-antigen into a mouse at a certain time after a previous identical self-antigen injection, the animals developed a fatal anaphylactic reaction. This phenomenon was dependent on whether the self-antigen is expressed in the thymus, where T cells develop. If the self-antigen is expressed in the thymus, then there cannot be an anaphylactic reaction. This study expands our view of autoimmunity and highlights the crucial role of the thymus in controlling the balance between autoimmunity and allergy. A News & Views was written on this paper by Howard Weiner of Harvard Medical School in Boston, MA. Lawrence Steinman
Stanford University
Beckman Center for Molecular Medicine, Room B002
Dept of Neurology and Neurological Sciences
Stanford, CA 94305-5316
Tel: +1 650 725-6401
Fax: +1 650 725-0627
Email: steinman@stanford.edu
Howard Weiner
Harvard Medical School
Center for Neurologic Diseases
Brigham and Women's Hospital
77 Ave Louis Pasteur, HIM 720
Boston, MA 02115
Tel: +1 617 525-5300
Fax: +1 617 525-5252
Email: weiner@cnd.bwh.harvard.edu
(C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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