       Document 0491
 DOCN  M9640491
 TI    Activation and re-activation potential of T cells responding to
       staphylococcal enterotoxin B.
 DT    9604
 AU    Hamel ME; Eynon EE; Savelkoul HF; van Oudenaren A; Kruisbeek AM;
       Division of Immunology, The Netherlands Cancer Institute,; Amsterdam.
 SO    Int Immunol. 1995 Jul;7(7):1065-77. Unique Identifier : AIDSLINE
       MED/96134430
 AB    To elucidate the parameters that lead to superantigen induced
       non-responsiveness, an in vitro model for studying primary and secondary
       responses to the bacterial superantigen staphylococcal enterotoxin B
       (SEB) was established. Upon re-activation with SEB, in vitro SEB primed
       T cells show an early proliferative response that 'quenches' in time and
       is severely impaired 3 days after re-stimulation. Despite their overall
       impaired proliferative capacity and IL-2 production, these T cells are
       able to produce IFN-gamma and to up-regulate activation markers CD69 and
       IL-2R alpha upon re-stimulation with SEB, demonstrating that SEB
       non-responsiveness is not absolute. Rather, it reflects the inability to
       mount an ongoing proliferative response upon re-stimulation with SEB.
       Our results also demonstrate that SEB-induced non-responsiveness is not
       simply the result of presentation in the absence of co-stimulation,
       since presentation of SEB on highly purified dendritic cells during the
       primary response did not prevent the induction of non-responsiveness. As
       previously shown, SEB induces a Th1 phenotype in responding CD4+ T
       cells. Skewing towards a Th2 phenotype by adding IL-4 and antibodies to
       IFN-gamma did not prevent the induction of non-responsiveness by SEB.
       Interestingly, T cells pretreated with plate-bound anti-CD3 epsilon and
       anti-V beta 8 were also non-responsive to SEB re-stimulation. Thus,
       non-responsiveness to SEB (defined here as inability to produce IL-2 and
       proliferate) seems to reflect an intrinsic inability of previously
       activated T cells to respond to SEB, probably reflecting differences in
       signal transduction pathways used by naive versus previously activated T
       cells.
 DE    Animal  Antigen-Presenting Cells/IMMUNOLOGY  B-Lymphocytes/IMMUNOLOGY
       Cells, Cultured  CD4-Positive T-Lymphocytes/METABOLISM  CD8-Positive
       T-Lymphocytes/METABOLISM  Dendritic Cells/IMMUNOLOGY
       Enterotoxins/*IMMUNOLOGY  Flow Cytometry  Immune Tolerance  Immunologic
       Memory/IMMUNOLOGY  Interferon Type II/AGONISTS/BIOSYNTHESIS
       Interleukin-2/BIOSYNTHESIS/PHARMACOLOGY  Interleukin-4/PHARMACOLOGY
       *Lymphocyte Transformation  Mice  Mice, Inbred BALB C  Mice, Inbred
       C57BL  Spleen/IMMUNOLOGY  Staphylococcus aureus/*IMMUNOLOGY
       Superantigens/*IMMUNOLOGY  Support, Non-U.S. Gov't
       T-Lymphocytes/*IMMUNOLOGY  Th2 Cells/METABOLISM  JOURNAL ARTICLE

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

