Abstract
Imiquimod (IMQ), a TLR7 agonist, is a standard local treatment for non-melanoma skin cancers (NMSC). IMQ triggers inflammation, ultimately resulting in immunological tumor destruction. Albeit IMQ promotes the recruitment of effector T (TE) cells, IMQ triggers anergy in CD4+ T cells. Meanwhile, how IMQ affects human CD8+ TE cells, pivotal to immunological cancer control, remains unclear. To address this, we studied CD8+ TE cell lines from NMSC and circulating, skin-homing CLA+CD8+ TE cells. In both models, IMQ-treated TE cells showed significantly reduced proliferation and IFN-γ production.
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