Document 0527
 DOCN  M9590527
 TI    T cells made deficient in interleukin-2 production by exposure to
       staphylococcal enterotoxin B in vivo are primed for interferon-gamma and
       interleukin-10 secretion.
 DT    9509
 AU    Florquin S; Amraoui Z; Goldman M; Laboratoire Pluridisciplinaire de
       Recherche Experimentale; Biomedicale, Hopital Erasme, Universite Libre
       de Bruxelles,; Belgium.
 SO    Eur J Immunol. 1995 May;25(5):1148-53. Unique Identifier : AIDSLINE
       MED/95293004
 AB    The superantigen staphylococcal enterotoxin B (SEB) induces a defect in
       interleukin (IL)-2 production by T cells expressing specific T cell
       receptor V beta domains. The present study was undertaken to determine
       the capacity of T cells, made deficient in IL-2 production by exposure
       to SEB in vivo, to secrete interferon (IFN)-gamma and IL-10 and to
       induce pathology upon SEB rechallenge. For this purpose, BALB/c mice
       received two intraperitoneal injections of 100 micrograms SEB with a
       48-h interval. First, we compared peak serum levels of IL-2, IFN-gamma
       and IL-10 after SEB rechallenge with those measured after a single SEB
       injection in control mice. The expected defect in IL-2 production in
       SEB-pretreated mice was associated with a major increase in IL-10 and
       IFN-gamma levels which were about fivefold higher than in controls.
       Experiments in mice depleted of CD4+ or CD8+ cells as well as studies in
       which purified T cell populations were rechallenged with SEB in vitro
       indicated that both CD4+ and CD8+ cells from SEB-pretreated mice were
       primed for IL-10 and IFN-gamma production. Furthermore, SEB-pretreated
       mice were sensitized to the toxic effects of the superantigen as
       indicated by a 30-70% lethality rate (vs. 0% in naive mice) within 48 h
       after SEB rechallenge. IFN-gamma was involved in the lethal syndrome as
       it could be prevented by injection of neutralizing anti-IFN-gamma
       monoclonal antibody. We conclude that SEB-reactive T cells made
       deficient for the production of IL-2 by exposure to SEB in vivo are
       primed for IFN-gamma and IL-10 production, and that IFN-gamma
       up-regulation is involved in the shock syndrome occurring upon SEB
       rechallenge.
 DE    Animal  Base Sequence  CD4-Positive T-Lymphocytes/DRUG EFFECTS/SECRETION
       CD8-Positive T-Lymphocytes/DRUG EFFECTS/SECRETION
       Enterotoxins/*PHARMACOLOGY/TOXICITY  Immune Tolerance  Interferon Type
       II/BIOSYNTHESIS/*SECRETION  Interleukin-10/BIOSYNTHESIS/*SECRETION
       Interleukin-2/*DEFICIENCY/GENETICS  Mice  Mice, Inbred BALB C  Molecular
       Sequence Data  Receptors, Antigen, T-Cell, alpha-beta  Specific
       Pathogen-Free Organisms  Superantigens/*PHARMACOLOGY  Support, Non-U.S.
       Gov't  T-Lymphocyte Subsets/*DRUG EFFECTS/SECRETION  JOURNAL ARTICLE

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