Abstract
Ng et al. have identified NKG7 as a regulator of inflammation in response to diverse immunological challenges. While NKG7 was required for the degranulation of cytotoxic cells, additional defects including reduced expansion and trafficking of CD8 T cells, and altered antigen presentation, were noted in NKG7-deficient mice. The precise mechanism by which NKG7 mediates its effects has not been resolved but may involve regulation of endosomal vesicle trafficking.
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