Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
Self-antigen-induced Th2 responses in experimental allergic encephalomyelitis (EAE)-resistant mice. Th2-mediated suppression of autoimmune disease.
J Immunol. 1995 Oct 15;155(8):4052-9. Unique Identifier : AIDSLINE MED/96003449 Cua DJ; Hinton DR; Stohlman SA; Department of Molecular Microbiology and Immunology, University; of Southern California School of Medicine, Los Angeles 90033,; USA.
Abstract:
Immunization of a limited number of rodent strains with central nervous system-derived Ags induces experimental allergic encephalomyelitis (EAE). In contrast to susceptible female SJL mice, age-matched males are resistant to actively induced EAE. The ability of immunization with neuroAg to induce Ag-specific T cell activation in resistant male mice was examined. Ag-specific T cell proliferation was found following immunization of both male and female SJL mice. Draining lymph node cytokine mRNA patterns demonstrated that immunization of EAE-resistant male mice resulted in a Th2-type pattern. By contrast, immunization of EAE-susceptible female mice resulted in a Th1-type pattern. Priming of Th1- and Th2-type responses was confirmed by analysis of cytokines secreted following Ag-specific proliferation. In contrast to the transfer of myelin basic protein (MBP)-specific Th1-type T cells derived from female mice, which induced acute and relapse EAE, transfer of MBP-specific Th2-type T cells derived from male mice resulted in no clinical or histologic evidence of EAE. A mixture of MBP-specific Th1 and Th2 type cells was transferred to naive recipients to determine if the neuroAg-specific Th2-type cells exerted a regulatory influence on EAE. Acute disease was partially eliminated and relapses were completely eliminated in these recipients. Analysis of spinal cords showed the presence of both Th1 and Th2 cytokine mRNAs. These data are consistent with both the ability of Th2-type cells to suppress autoimmunity and a homeostatic mechanism of T cell regulation based on the cross-regulation of Th1 and Th2 cells in the maintenance of peripheral tolerance.
Keywords: Animal Autoantigens/*IMMUNOLOGY Disease Susceptibility Encephalomyelitis, Allergic/ETIOLOGY/*IMMUNOLOGY/THERAPY Female Immunity, Natural Immunotherapy, Adoptive *Lymphocyte Transformation Male Mice Mice, Inbred Strains Myelin Basic Proteins/IMMUNOLOGY Self Tolerance Support, Non-U.S. Gov't Th2 Cells/*IMMUNOLOGY JOURNAL ARTICLE
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Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
