Abstract
Tissue-resident memory T cells (TRM) provide optimal defense at sites of infection, but signals regulating their development are unclear, especially for CD4 T cells. Here, we identify two distinct pathways that lead to the generation of CD4 TRM in the lungs following influenza infection. The TRM are transcriptionally distinct from conventional memory CD4 T cells, and share a gene signature with CD8 TRM. The CD4 TRM are superior cytokine producers compared to conventional memory cells, can protect otherwise naïve mice against a lethal influenza challenge, and display functional specialization by inducing enhanced inflammatory responses from dendritic cells compared to conventional memory cells. Finally, we demonstrate than an IL-2-dependent and a novel IL-2-independent but IL-15-dependent pathway support the generation of cohorts of lung TRM.
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