Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học General Psychiatry cung cấp cho các bạn kiến thức về ngành y đề tài: γ Paradoxical roles of IFN-γ in models of Th1-mediated autoimmunity. | Available online http content 4 6 333 Commentary Paradoxical roles of IFN-y in models of Thl-mediated autoimmunity Edward F Rosloniec1 2 3 Kary Latham3 and Yajaira B Guedez2 1VA Medical Center Research Service 151 Memphis Tennessee USA 2Department of Medicine University of Tennessee Health Science Center Memphis Tennessee USA 3Department of Pathology University of Tennessee Health Science Center Memphis Tennessee USA Corresponding author Edward F Rosloniec e-mail erosloniec@ Received 13 May 2002 Revisions received 3 July 2002 Accepted 3 July 2002 Published 17 July 2002 Arthritis Res 2002 4 333-336 DOI 2002 BioMed Central Ltd Print ISSN 1465-9905 Online ISSN 1465-9913 Abstract T-cell responses to antigens are classified on the basis of the cytokines they produce as either Th1 IFN-y IL-2 or Th2 IL-4 IL-10 with these Th types being indicative of either cell-mediated or antibody-mediated responses respectively. Using this classification T-cell responses in MHC-class-II-restricted autoimmune diseases appear to be predominantly of the Th1 type based on the presence of high levels of IFN-y. This simplistic classification has recently been challenged however as disease incidence and severity are frequently elevated in animals that have a deficient IFN-y response. The recent data discussed here indicate that the cytokine circuits involved in the regulation of cell-mediated and humoral immune responses during the development of autoimmune arthritis are more complex than originally proposed perhaps our characterization of autoimmune responses as strictly Th1 or Th2 is overly simplistic especially as it pertains to the role of IFN-y. Keywords arthritis autoimmunity cytokines IFN-y Introduction Cytokines play critical roles in regulating the outcome of antigen-specific T-cell responses and thus have been a major focus in the study of the pathogenesis of autoimmunity. On the basis of the original description by Mosmann et al. 1 we .
