在癌症患者中，肿瘤引流淋巴结中的树突状细胞（DCs）能以打破免疫耐受的方式呈递抗原给原始T细胞。感染后T细胞的克隆扩增子在肿瘤部位进一步受到DCs的调控。肿瘤内的DCs既能提供生存信号给T细胞，又能驱动来袭T细胞的效应分化，从而局部增强抗肿瘤免疫力。然而，肿瘤内DCs的稀缺性或其表达免疫调节分子经常限制抗肿瘤T细胞反应。在本文中，我们回顾了目前对原发和效应免疫反应部位的DC-T细胞相互作用的理解。我们将新兴洞察力纳入到肿瘤免疫中的DC功能、发生和其他环境中的功能等方面进行讨论，并提出DCs控制癌症免疫循环中至少两个与T细胞相关的检查点的观点。我们对这两个检查点的理解对于开发新的癌症免疫疗法有重要意义。版权所有©2023年Elsevier Inc.。保留所有权利。

In cancer patients, dendritic cells (DCs) in tumor-draining lymph nodes can present antigens to naive T cells in ways that break immunological tolerance. The clonally expanded progeny of primed T cells are further regulated by DCs at tumor sites. Intratumoral DCs can both provide survival signals to and drive effector differentiation of incoming T cells, thereby locally enhancing antitumor immunity; however, the paucity of intratumoral DCs or their expression of immunoregulatory molecules often limits antitumor T cell responses. Here, we review the current understanding of DC-T cell interactions at both priming and effector sites of immune responses. We place emerging insights into DC functions in tumor immunity in the context of DC development, ontogeny, and functions in other settings and propose that DCs control at least two T cell-associated checkpoints of the cancer immunity cycle. Our understanding of both checkpoints has implications for the development of new approaches to cancer immunotherapy.Copyright © 2023 Elsevier Inc. All rights reserved.