Document 0291
 DOCN  M9650291
 TI    ICAM-1 is required for T cell proliferation but not for anergy or
       apoptosis induced by Staphylococcus aureus enterotoxin B in vivo.
 DT    9605
 AU    Gonzalo JA; Martinez C; Springer TA; Gutierrez-Ramos JC; Center for
       Blood Research, Harvard Medical School, Boston, MA; 02115, USA.
 SO    Int Immunol. 1995 Oct;7(10):1691-8. Unique Identifier : AIDSLINE
       MED/96128663
 AB    The response of T lymphocytes to superantigens requires expression of
       the appropriate TCR V beta gene products as well as the establishment of
       cellular interactions mediated by adhesion molecules. To study the role
       of intercellular adhesion molecule (ICAM)-1 in the response in vivo to
       superantigens, we have analyzed the effects induced by the bacterial
       superantigen Staphylococcus aureus enterotoxin B (SEB) in mice which
       have been made genetically deficient in ICAM-1. SEB treatment of
       wild-type mice causes proliferation, deletion and anergy of the
       SEB-reactive V beta 8+ T cell population. Here we show that cellular
       interactions mediated by ICAM-1 are not essential for the induction of
       anergy or for the deletion of CD4+ V beta 8+ or CD8+ V beta 8+ T cells,
       but are required for the proliferation of these peripheral T
       lymphocytes. This is the first demonstration in vivo that the absence of
       the co-stimulatory signals provided by the interaction of ICAM-1 with
       its specific ligands impairs the proliferation of SEB-reactive T cells.
       Interestingly, our study showed that SEB-induced proliferation of CD8+ V
       beta 8+ T cells from lymph nodes (not from spleen) is independent of the
       interactions mediated by ICAM-1.
 DE    Animal  Antigens, Bacterial/*IMMUNOLOGY  Apoptosis/*PHYSIOLOGY  Cell
       Division/PHYSIOLOGY  Cells, Cultured  Clonal Anergy/*PHYSIOLOGY
       Comparative Study  CD4-Positive T-Lymphocytes/*IMMUNOLOGY  CD8-Positive
       T-Lymphocytes/*IMMUNOLOGY  Enterotoxins/*IMMUNOLOGY  Human
       Intercellular Adhesion Molecule-1/GENETICS/*PHYSIOLOGY  Lymph
       Nodes/CYTOLOGY  Lymphocyte Transformation/*PHYSIOLOGY  Mice  Mice,
       Inbred C57BL  Mice, Mutant Strains  Organ Specificity  Receptors,
       Antigen, T-Cell, alpha-beta/GENETICS  Specific Pathogen-Free Organisms
       Spleen/CYTOLOGY  Staphylococcus aureus/IMMUNOLOGY
       Superantigens/*IMMUNOLOGY  Support, Non-U.S. Gov't  JOURNAL ARTICLE

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