摘要：

Summary Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers \{DC\} activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through \{TAM\} receptor tyrosine kinases in \{DCs\} to limit the magnitude of \{DC\} activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in \{DCs\} and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, \{PROS1\} was expressed in activated human T cells, and its ability to regulate \{DC\} activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.

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