Vβ11+T-lymphocyte expansion by toxic shock syndrome toxin-1 differs in mice bearing H-2qversus H-2bhaplotypes

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Abstract
We have recently demonstrated that toxic shock syndrome toxin-1 (TSST-1) expanded Vβ11+ T lymphocytes contribute to Staphylococcus aureus arthritis and sepsis-induced mortality. Interestingly, Vβ11+ T-cell mediated joint pathology varies in different mouse strains. In this study, we characterized the in vitro pattern of Vβ11+ T-cell expansion by TSST-1 in mice with various genetic backgrounds. Mice expressing major histocompatibility complex (MHC) class II I-E molecules did not expand Vβ11+ T cells upon stimulation with TSST-1. Using B10 congeneic I-E negative mouse strains, we found that the TSST-1-expanded Vβ11+ T cells in B10Q (H-2q) and B10M (H-2f) mice but not in B10B (H-2b) mice. Antigen-presenting cells (APC) from B10Q mice, L cells and lymphoma cell line transfected with a q gene did not restore the deficient Vβ11+ T-cell expansion by TSST-1 in purified T cells from B10B mice. In contrast, I-Ab APC were able to stimulate Vβ11+ T cells from H-2q mice. Furthermore, Vβ11+ T cells in H-2b mice did expand when exposed to staphylococcal enterotoxin A (SEA). These findings suggest that the T-cell repertoire, skewed by clonal deletion and inactivation of self-reactive T cells, accounts for the different magnitude of Vβ11+ T-cell expansion among the different mouse strains.