Document 0416
 DOCN  M9550416
 TI    Staphylococcal enterotoxin B modulates V beta 8+ TcR-associated T-cell
       memory against conventional antigen.
 DT    9505
 AU    Bell SJ; Buxser SE; Section of Allergy/Immunology, East Carolina
       University School of; Medicine, Greenville, North Carolina 27858.
 SO    Cell Immunol. 1995 Jan;160(1):58-64. Unique Identifier : AIDSLINE
       MED/95144750
 AB    Primary in vivo challenge with the superantigen staphylococcal
       enterotoxin B (SEB) induces polyclonal proliferation of an unusually
       large proportion of circulating T-cells that bear the V beta 8-T-cell
       receptor (TcR) domain. Early and vigorous proliferation of V beta 8+
       T-cells precedes their selective deletion, leaving the host unresponsive
       upon rechallenge with the native immunogen SEB. Nonetheless, this
       induction of anergy is incompletely understood. Recently we demonstrated
       that more cells than just V beta 8+ T-cells undergo clonal proliferation
       after challenge with SEB (Cell. Immunol. 154, 440, 1994). These findings
       suggested that non-V beta 8+ T-cells may have a role in the induction of
       superantigen-induced anergy. To further investigate this, we enumerated
       CD4+ and CD8+ T-cells in lymph nodes and spleens from Balb/c mice at
       various times after primary and secondary challenge with either a high
       or a low dose of SEB. Using these kinetic data we investigated whether
       challenge with SEB would modulate antigen-specific V beta 8-associated
       T-memory responses. To this end, the V beta 8+ T-cell-associated
       responses induced by SEB were compared with the V beta 8+ TcR-associated
       memory responses induced by the nominal antigen sperm whale myoglobin
       (SWM). Results indicated that challenge of SWM-primed mice with SEB
       abrogated the V beta 8-associated SWM-specific T-cell memory for an
       extended but transient period of time. Moreover, prechallenge with SEB
       blocked the establishment of de novo V beta + T-cell-mediated immunity.
       These findings suggest that administration of low and controlled doses
       of microbial superantigen could provide long-term suppression of
       antigen-specific cell-mediated immunity.
 DE    Animal  Clonal Anergy/*IMMUNOLOGY  CD4-Positive T-Lymphocytes/IMMUNOLOGY
       CD8-Positive T-Lymphocytes/*IMMUNOLOGY  Enterotoxins/IMMUNOLOGY  Female
       Flow Cytometry  Immunologic Memory/*IMMUNOLOGY  Lymphocyte
       Transformation/IMMUNOLOGY  Mice  Mice, Inbred BALB C
       Myoglobin/IMMUNOLOGY  Receptors, Antigen, T-Cell, alpha-beta/*IMMUNOLOGY
       Superantigens/*IMMUNOLOGY  JOURNAL ARTICLE

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