Staphylococcal enterotoxin-B-induced lethal shock in mice is T-cell-dependent, but disease susceptibility is defined by the non-T-cell compartment
Copyright 2001 Academic Press.
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 98(2001), 1 vom: 01. Jan., Seite 85-94 |
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| Auteur principal: | |
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| Format: | Article |
| Langue: | English |
| Publié: |
2001
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Enterotoxins Tumor Necrosis Factor-alpha enterotoxin B, staphylococcal 39424-53-8 |
| Résumé: | Copyright 2001 Academic Press. Here we introduce a murine model for SEB-induced lethal shock that relies on the administration of SEB alone and does not involve hepatotoxicity by avoiding pretreatment with the hepatotoxin D-galactosamine. In the absence of D-gal, we first identified SEB-susceptible and -resistant H-2(k)-congenic mouse strains. In contrast with what is well established for the classic D-gal-dependent model and what therefore is anticipated for the human disease, the levels of TNF produced did not define susceptibility in our model. The SEB-induced TNF response in vitro and in vivo was stronger in resistant B10.BR mice than in susceptible C3H/HeJ mice. Neither the magnitude nor the quality of the T cell response induced by SEB defined susceptibility. Adoptive transfer experiments in C3H-SCID recipient mice demonstrated that induction of the disease is T-cell-dependent. T cells from resistant and susceptible mice both transferred disease susceptibility to H-2(k)-congenic C3H-SCID mice, indicating that disease susceptibility is downstream from T cell activation, at the level of the target organ itself, which responds differently to T-cell-induced inflammation |
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| Description: | Date Completed 22.02.2001 Date Revised 21.11.2008 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |