Document 0642
 DOCN  M9620642
 TI    Normal clonal expansion but impaired Fas-mediated cell death and anergy
       induction in interleukin-2-deficient mice.
 DT    9602
 AU    Kneitz B; Herrmann T; Yonehara S; Schimpl A; Institute of Virology and
       Immunobiology, Wurzburg, Germany.
 SO    Eur J Immunol. 1995 Sep;25(9):2572-7. Unique Identifier : AIDSLINE
       MED/96011869
 AB    Despite a normal development of all major lymphoid subsets, with time,
       interleukin-2 (IL-2)-deficient mice develop a fatal immunopathology. The
       disease phenotype is characterized by lymphoadenopathy, splenomegaly, T
       cell infiltration of various organs, overproduction of a number of
       cytokines and autoantibody formation. Phenotypically, CD4+ and CD8+ T
       cells exhibit features characteristic of antigenically experienced
       cells. The accumulation of cells with a memory phenotype together with
       the previous suggestion of an involvement of IL-2 in the termination
       phase of immune responses prompted us to study the fate of
       superantigen-reactive T cells in IL-2-deficient mice in comparison to
       their IL-2-producing littermates. We show that expansion in vivo of CD4+
       and, to a lesser extent, CD8+ T cells reactive to the superantigens
       staphylococcal enterotoxin A and B (SEA and SEB) proceeds normally in
       the absence of IL-2, but that fewer CD4+ cells are subsequently deleted.
       The residual superantigen-reactive cells fail to become anergic as
       measured by proliferation in vitro in response to the same superantigen.
       T cell blasts generated in vitro from lymph node cells of IL-2-deficient
       mice by superantigen stimulation in the absence of exogenous IL-2 also
       fail to become anergic. In contrast to cells from IL-2-producing
       littermates, they do not exhibit Fas-induced apoptosis when cultured on
       anti-Fas antibody-coated plates, although Fas expression by
       IL-2-deficient cells is normal or even elevated compared to the
       IL-2-producing control cells. The data suggest that activation of T
       cells in the absence of IL-2 fails to generate a signal which is
       necessary to activate the apoptotic pathway and thus leads to an
       accumulation of antigen-experienced cells and the chronic inflammatory
       responses observed in IL-2-deficient mice.
 DE    Animal  Antigens, CD95/*IMMUNOLOGY  Apoptosis/IMMUNOLOGY  Cell
       Differentiation  CD4-Positive T-Lymphocytes/*IMMUNOLOGY  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY  Enterotoxins/IMMUNOLOGY
       Interleukin-2/*DEFICIENCY  Mice  Superantigens/IMMUNOLOGY  Support,
       Non-U.S. Gov't  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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