In this issue of JEM, Sparano et al. (https://doi.org/10.1084/jem.20240930) present compelling evidence that salivary gland trNK cells originate from cNK cells and are developmentally distinct from ILC1 cells. Mechanistically, they demonstrate that continuous autocrine TGF-β signaling drives salivary gland tissue residency and works in synergy with IL-15 to enhance Hobit-dependent cytotoxicity.
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