KLRD1 and infection: Ninety-four percent of genes that distinguished this adaptive-like Vδ1 population (P < 5.2e–05, linear model, likelihood ratio test, Bonferroni threshold) were adaptiveness and innateness genes, including downregulated cytotoxic genes, such as PRF1 and KLRD1, and upregulated ribosomal machinery genes, such as RPL34, RPL22, and EEF1A1. This finding is consistent with recent reports on Vδ1 populations being highly variable across donors, and with dynamic changes in response to infection, suggesting that a naive Vδ1 state may be part of their development52,53.