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Steele, Maria M; Jaiswal, Abhinav; Delclaux, Ines; Dryg, Ian D; Murugan, Dhaarini; Femel, Julia; Son, Sunny; du Bois, Haley; Hill, Cameron; Leachman, Sancy A; Chang, Young H; Coussens, Lisa M; Anandasabapathy, Niroshana; Lund, Amanda W
Nature immunology, 04/2023, Volume: 24, Issue: 4Journal Article
Antigen-specific CD8 T cell accumulation in tumors is a prerequisite for effective immunotherapy, and yet the mechanisms of lymphocyte transit are not well defined. Here we show that tumor-associated lymphatic vessels control T cell exit from tumors via the chemokine CXCL12, and intratumoral antigen encounter tunes CXCR4 expression by effector CD8 T cells. Only high-affinity antigen downregulates CXCR4 and upregulates the CXCL12 decoy receptor, ACKR3, thereby reducing CXCL12 sensitivity and promoting T cell retention. A diverse repertoire of functional tumor-specific CD8 T cells, therefore, exit the tumor, which limits the pool of CD8 T cells available to exert tumor control. CXCR4 inhibition or loss of lymphatic-specific CXCL12 boosts T cell retention and enhances tumor control. These data indicate that strategies to limit T cell egress might be an approach to boost the quantity and quality of intratumoral T cells and thereby response to immunotherapy.
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