1c:I[419806,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/1270dead247da766.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/2d7aa753e81324a8.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/263f2cdcb9aa2341.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 1d:T4f3,In tumors, a subset of CD8⁺ T cells expressing the transcription factor TCF-1 drives the response to immune checkpoint blockade. We examined the mechanisms that maintain these cells in an autochthonous model of lung adenocarcinoma. Longitudinal sampling and single-cell sequencing of tumor-antigen specific TCF-1⁺ CD8⁺ T cells revealed that while intratumoral TCF-1⁺ CD8⁺ T cells acquired dysfunctional features and decreased in number as tumors progressed, TCF-1⁺ CD8⁺ T cell frequency in the tumor draining LN (dLN) remained stable. Two discrete intratumoral TCF-1⁺ CD8⁺ T cell subsets developed over time-a proliferative SlamF6⁺ subset and a non-cycling SlamF6^- subset. Blocking dLN egress decreased the frequency of intratumoral SlamF6⁺ TCF-1⁺ CD8⁺ T cells. Conventional type I dendritic cell (cDC1) in dLN decreased in number with tumor progression, and Flt3L+anti-CD40 treatment recovered SlamF6⁺ T cell frequencies and decreased tumor burden. Thus, cDC1s in tumor dLN maintain a reservoir of TCF-1⁺ CD8⁺ T cells and their decrease contributes to failed anti-tumor immunity.

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