New findings reported from University of Maryland, Medical Department describe advances in arthritis
2008 JAN 14 -- "In autoimmune situations, the outcome of immune response against a disease-related antigen is typically viewed in terms of the balance between the pathogenic versus the protective subsets of antigen-reactive T cells. Using the rat adjuvant arthritis (AA) model of human rheumatoid arthritis (RA), we examined the antigen specificity and the functional attributes of the T cell repertoire directed against defined pathogenic versus protective epitopes of heat-shock protein 65 (hsp65), and determined the immunologic basis of the AA-protective effect of subsets of T cells primed by the pathogenic determinant," investigators in the United States report. "Lewis (RT.1(1)) rats were pretreated subcutaneously with the pathogenic epitope 177-191 of mycobacterial hsp65 (13177) in adjuvant (incomplete Freund's adjuvant/complete Freund's adjuvant/CpG) and then immunized with heat-killed M. tuberculosis H37Ra for disease induction. The antigen specificity/crossreactivity of the T cells primed by B177 or the AA-protective determinant 465-479 of the homologous rat hsp65 (R465) was tested by using proliferation assay, cytokine ELISA, tolerance induction, and adoptive transfer. Pretreatment of Lewis rats with the arthritogenic determinant B 177 using an immunogenic rather than a tolerogenic regimen affords protection against AA instead of initiation or aggravation of AA. This protective effect of B 177 is mediated in part by activation of T cells that are crossreactive with R465," wrote M. Durai and colleagues, University of Maryland, Medical Department. The researchers concluded: "Downmodulation of AA by a pathogenic foreign epitope involving T cells crossreactive with a distant, protective self-determinant represents a novel aspect of immune regulation, and suggests further exploration of the use of pathogenic epitopes for the treatment of autoimmune arthritis." Durai and colleagues published their study in the Journal of Rheumatology (T cells against the pathogenic and protective epitopes of heat-shock protein 65 are crossreactive and display functional, similarity: Novel aspect of regulation of autoimmune arthritis. Journal of Rheumatology, 2007;34(11):2134-2143). For additional information, contact K.D. Moudgil, University of Maryland, School Medical, Dept. of Microbiology & Immunology, Howard Hall 323C, 660 W Redwood St., Baltimore, MD 21201, USA. The publisher of the Journal of Rheumatology can be contacted at: J Rheumatol Publ Co., 920 Yonge St., Suite 115, Toronto, Ontario M4W 3C7, Canada. Keywords: United States, Baltimore, Arthritis, Autoimmune Disease, Autoimmune Disorder, Autoimmunity, Cutaneous Tuberculosis, Immunology, Mycobacteria, Mycobacterium Tuberculosis, Rheumatoid Arthritis, Rheumatology, University of Maryland, Medical Department. This article was prepared by Tuberculosis Week editors from staff and other reports. Copyright 2008, Tuberculosis Week via NewsRx.com.
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