A core feature of protective T cell responses to infection is the robust expansion and diversification of naïve antigen-specific T cell populations into short-lived effector and long-lived memory subsets. By means of in vivo fate mapping, we found a striking variability of immune responses derived from individual CD8(+) T cells and show that robust acute and recall immunity requires the initial recruitment of multiple precursors. Unbiased mathematical modeling identifies the random integration of multiple differentiation and division events as the driving force behind this variability. Within this probabilistic framework, cell fate is specified along a linear developmental path that progresses from slowly proliferating long-lived to rapidly expanding short-lived subsets. These data provide insights into how complex biological systems implement stochastic processes to guarantee robust outcomes.
Fate mapping of single NK cells identifies a type 1 innate lymphoid-like lineage that bridges innate and adaptive recognition of viral infection Graphical abstract Highlights d Adaptive-like NK cell responses to MCMV encompass conventional and ILC1-like lineages d ILC1-like NK cells show enhanced cytokine production and splenic residency d ILC1-like NK cells show EOMES expression, target-specific cytotoxicity, and clonal expansion d ILC1-like NK cells drive cDC1 clustering and CD8 + T cell priming dependent on Ly49H and Batf3
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