STAT3 regulates cytotoxicity of human CD57+ CD4+ T cells in blood and lymphoid follicles.

A subset of human follicular helper T cells (TFH) cells expresses CD57 for which no distinct function has been identified. We show that CD57+ TFH cells are universally PD-1^hi, but compared to their CD57- PD-1^hi counterparts, express little IL-21 or IL-10 among others. Instead, CD57 expression on TFH cells marks cytotoxicity transcriptional signatures that translate into only a weak cytotoxic phenotype. Similarly, circulating PD-1+ CD57+ CD4+ T cells make less cytokine than their CD57- PD-1+ counterparts, but have a prominent cytotoxic phenotype. By analysis of responses to cytokines and cells from patients with gain- or loss-of-function mutations, we show that CD4+ T cell cytotoxicity is TFH formation also requires but paradoxically, once formed, PD-1^hi cells become unresponsive to These findings suggest that changes in blood and germinal center cytotoxicity might be affected by changes in duanyu18133 signaling, or modulation of PD-1 by therapy.

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