{Reference Type}: Journal Article
{Title}: Collaboration between IL-7 and IL-15 enables adaptation of tissue-resident and circulating memory CD8+ T cells.
{Author}: Jarjour NN;Dalzell TS;Maurice NJ;Wanhainen KM;Peng C;DePauw TA;Block KE;Valente WJ;Ashby KM;Masopust D;Jameson SC;
{Journal}: bioRxiv
{Volume}: 0
{Issue}: 0
{Year}: 2024 Jun 3
暂无{DOI}: 10.1101/2024.05.31.596695
{Abstract}: Interleukin-7 (IL-7) is considered a critical regulator of memory CD8+ T cell homeostasis, but this is primarily based on analysis of circulating and not tissue-resident memory (TRM) subsets. Furthermore, the cell-intrinsic requirement for IL-7 signaling during memory homeostasis has not been directly tested. Using inducible deletion, we found that Il7ra loss had only a modest effect on persistence of circulating memory and TRM subsets and that IL-7Rα was primarily required for normal basal proliferation. Loss of IL-15 signaling imposed heightened IL-7Rα dependence on memory CD8+ T cells, including TRM populations previously described as IL-15-independent. In the absence of IL-15 signaling, IL-7Rα was upregulated, and loss of IL-7Rα signaling reduced proliferation in response to IL-15, suggesting cross-regulation in memory CD8+ T cells. Thus, across subsets and tissues, IL-7 and IL-15 act in concert to support memory CD8+ T cells, conferring resilience to altered availability of either cytokine.