       Document 0401
 DOCN  M9610401
 TI    Self-antigen-induced Th2 responses in experimental allergic
       encephalomyelitis (EAE)-resistant mice. Th2-mediated suppression of
       autoimmune disease.
 DT    9601
 AU    Cua DJ; Hinton DR; Stohlman SA; Department of Molecular Microbiology and
       Immunology, University; of Southern California School of Medicine, Los
       Angeles 90033,; USA.
 SO    J Immunol. 1995 Oct 15;155(8):4052-9. Unique Identifier : AIDSLINE
       MED/96003449
 AB    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.
 DE    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

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

