Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
Activation and re-activation potential of T cells responding to staphylococcal enterotoxin B.
Int Immunol. 1995 Jul;7(7):1065-77. Unique Identifier : AIDSLINE MED/96134430 Hamel ME; Eynon EE; Savelkoul HF; van Oudenaren A; Kruisbeek AM; Division of Immunology, The Netherlands Cancer Institute,; Amsterdam.
Abstract:
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.
Keywords: 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 960430
M9640840
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Important note: Information in this article was accurate in 1996. The state of the art may have changed since the publication date.
