Critical role of T cell migration in bacterial superantigen-mediated shock in mice
Bacterial superantigens have been implicated in the pathogenesis of several human diseases. Among them, toxic shock syndrome (TSS) is a prototypic acute intoxication caused by the pyrogenic exotoxin family of superantigens. In this study, we investigated the pathophysiological mechanism of TSS using...
| Veröffentlicht in: | Clinical immunology (Orlando, Fla.). - 1999. - 110(2004), 2 vom: 14. Feb., Seite 159-71 |
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| 1. Verfasser: | |
| Weitere Verfasser: | , , , , , , |
| Format: | Aufsatz |
| Sprache: | English |
| Veröffentlicht: |
2004
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| Zugriff auf das übergeordnete Werk: | Clinical immunology (Orlando, Fla.) |
| Schlagworte: | Journal Article Bacterial Proteins Superantigens Tumor Necrosis Factor-alpha Yersinia pseudotuberculosis-derived mitogen Interleukin-10 130068-27-8 Interferon-gamma 82115-62-6 |
| Zusammenfassung: | Bacterial superantigens have been implicated in the pathogenesis of several human diseases. Among them, toxic shock syndrome (TSS) is a prototypic acute intoxication caused by the pyrogenic exotoxin family of superantigens. In this study, we investigated the pathophysiological mechanism of TSS using the Yersinia pseudotuberculosis-derived mitogen (YPM) and its point mutants. The results indicated that YPM could induce toxic shock in BALB/c mice but not in T cell-deficient SCID mice. We found that Vbeta8(+) T cells activated by YPM migrated from peripheral blood to liver as early as 1 h after injection of YPM and that serum level of IFN-gamma was significantly elevated 4 h after YPM injection. Co-administration of anti-IFN-gamma antibody or anti-YPM monoclonal antibody alleviated the liver injury and protected mice from YPM-induced death. Moreover, anti-YPM antibody also suppressed the early migration of Vbeta8(+) T cells from the peripheral circulation and the elevation of serum IFN-gamma level, indicating a pivotal role of T cells in inducing shock in our mouse model |
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| Beschreibung: | Date Completed 15.04.2004 Date Revised 21.11.2008 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |