期刊
JOURNAL OF IMMUNOLOGY
卷 165, 期 11, 页码 6056-6066出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.165.11.6056
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资金
- NIAID NIH HHS [AI4666, AI26887] Funding Source: Medline
We have previously shown that systemic staphylococcal enterotoxin A (SEA) injections cause CD4 T cells in TCR-transgenic mice to become tolerant to subsequent ex vivo restimulation. An active IFN-gamma -dependent mechanism of suppression was responsible for the apparent unresponsiveness of the CD4 T cells. In this study, me analyze the response of CD4 T cells isolated throughout the first 10 days of the in vivo response to injected SEA. We show that CD4 T cells isolated at the peak of the in vivo response undergo very little activation-induced cell death after sterile FAGS sorting or restimulation in the presence of neutralizing Abs to IFN-gamma, We also show that the IFN-gamma -dependent tolerance develops soon after SEA injection in the spleens of both normal and TCR-transgenic mice. This suppression is dependent upon myeloid cells from the SEA-treated mice and is optimal when inducible NO synthase activity and reactive oxygen intermediates are both present. The data indicate that IFN-gamma, myeloid cells, and a combination of NO and reactive oxygen intermediates all contribute to a common pathway of T cell death that targets activated or responding CD4 T cells. Sorted Gr-1(+) cells from SEA-treated mice also directly suppress the response of naive CD4 T cells in mixed cultures, indicating that this tolerance mechanism may play a role in down-regulating other vigorous immune responses.
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