A minority of Th1 and Tfh effector cells express survival genes shared by memory cell progeny and require IL-7 or TCR signaling to persist.

Abstract

It is not clear how CD4+ memory T cells are formed from a much larger pool of earlier effector cells. We found that transient systemic bacterial infection rapidly generates several antigen-specific Th1 and T follicular helper (Tfh) effector cell populations with different tissue residence behaviors. Each Th1 and Tfh effector cell type produced a similar memory cell type, which was maintained by IL-7, or in the case of germinal center Tfh cells, by the T cell antigen receptor (TCR). Although most cells of all varieties had transcriptomes indicative of cell stress and death at the peak of the response, some had already acquired a quiescence signature. This thesis demonstrates that acute infection induces differentiation of Th1 and Tfh effector cells, a minority of which quickly adopt a transcriptional program that allows escape from death and become memory cells that survive from sensing IL-7 or a TCR ligand.