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Homeostatic proliferation of naïve CD8+ T cells depends on CD62L/L‐selectin‐mediated homing to peripheral LN

Adoptive transfer of naïve CD8+ T cells into lymphopenic recipients results both in spontaneous proliferation and in partial activation of T cells, a phenomenon termed homeostatic proliferation (HP). HP of CD8+ T cells is dependent on host IL‐7, IL‐15, and MHC‐class I and has been shown to prevent T‐cell tolerance, reverse T‐cell anergy and support T‐cell‐mediated tumor control in vivo. However, the initial anatomic site of HP is still under debate. Since we observed that the earliest detectable HP occurs within LN and that T cells undergoing HP retain a CD62Lbright phenotype, we investigated the functional role of CD62L for this process. We found that CD62L‐expression on T cells is required for optimal HP and HP was impaired in lymphotoxin‐αβ−/− mice, indicating the necessity for intact host secondary lymphoid organ structures. Use of the LN egression inhibitor FTY720 indicated that LN structures were pivotal to yield homeostatically proliferated T cells detected in other compartments. Consistent with these results, HP‐supported control of MC57‐SIY tumors depended on CD62L. Our data indicate a critical role for CD62L and LN homing for the process of HP, which has implications for adoptive immunotherapy approaches of cancer.