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In This Issue, The Journal of Immunology, Volume 177, Issue 12, December 2006, Pages 8281–8282, https://doi.org/10.4049/jimmunol.177.12.8281
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T Cells in Innate Immunity
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The observation that STAT proteins are crucial in innate immunity during septic peritonitis in mice prompted Watanabe et al. (p. 8650 ) to look at the role of suppressors of cytokine signaling (SOCS) proteins in attenuating responses of cytokines that act through the JAK/STAT pathway. They found that mice transgenic for SOCS5 (SOCS5Tg) had higher survival rates and increased bacterial clearance after sepsis induced by cecal ligation and puncture (CLP) than wild-type controls; transgenic neutrophils and macrophages infected in vitro produced more superoxide and killed more bacteria than wild-type cells. SOCS5Tg mice had greater infiltration of peritoneal leukocytes with reduced STAT6 phosphorylation and had higher IL-12, IFN-γ, and TNF-α levels in peritoneal exudates after CLP. Wild-type phagocytes cocultured with transgenic CD4+ T cells killed more bacteria than phagocytes cocultured with wild-type CD4+ T cells. RAG−/− mice adoptively transferred with CD4+ T cells before CLP had more peritoneal leukocytes and fewer bacteria than mice given wild-type cells. Anti-IFN-γ Ab abrogated the increased LPS-stimulated production of TNF-α of wild-type macrophages cocultivated with SOCS5Tg vs wild-type CD4+ T cells. Transgenic mice had more peripheral memory T cells and fewer naive T cells than controls. Histological examination of SOCS5Tg kidneys after CLP revealed minimal damage. The authors propose that CD4+ T cells overexpressing SOCS5 protein enhance innate immune responses during CLP by IFN-γ-induced activation of leukocytes.
