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Paradoxical roles of IFN-γ in models of Th1-mediated autoimmunity 英文参考文献
Available online /content/4/6/333
Commentary
Paradoxical roles of IFN-γ in models of Th1-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 10.1186.ar432)
? 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-γ, 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-γ. This simplistic classification has recently been challenged, however, as disease
incidence and severity are frequently elevated in animals that have a deficient IFN-γ 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-γ.
Keywords: arthritis, autoimmunity, cytokines, IFN-γ
Introduction
Most autoimmune diseases and models of autoimmunity in
which susceptibility is associated with the expression of
specific MHC class II allotypes appear to be of the
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