The efficacy of checkpoint immunotherapy to non-small cell lung cancer (NSCLC) largely depends on the tumor microenvironment (TME). Here, we demonstrate that CCL7 facilitates anti-PD-1 therapy for the Kras^LSL−G12D/+Tp53^fl/fl (KP) and the Kras^LSL−G12D/+Lkb1^fl/fl (KL) NSCLC mouse models by recruiting conventional DC 1 (cDC1) into the TME to promote T cell expansion. CCL7 exhibits high expression in NSCLC tumor tissues and is positively correlated with the infiltration of cDC1 in the TME and the overall survival of NSCLC patients. CCL7 deficiency impairs the infiltration of cDC1 in the TME and the subsequent expansion of CD8⁺ and CD4⁺ T cells in bronchial draining lymph nodes and TME, thereby promoting tumor development in the KP mouse model. Administration of CCL7 into lungs alone or in combination with anti-PD-1 significantly inhibits tumor development and prolongs the survival of KP and KL mice. These findings suggest that CCL7 potentially serves as a biomarker and adjuvant for checkpoint immunotherapy of NSCLC.

关卡免疫疗法对非小细胞肺癌（NSCLC）的疗效在很大程度上取决于肿瘤微环境（TME）。在这里，我们证明了CCL7通过募集常规DC促进Kras ^{LSL-G12D / +} Tp53 ^{fl / fl}（KP）和Kras ^{LSL-G12D / +} Lkb1 ^{fl / fl}（KL）NSCLC小鼠模型的抗PD-1治疗1（cDC1）进入TME以促进T细胞扩增。CCL7在NSCLC肿瘤组织中高表达，并与TME中cDC1的浸润和NSCLC患者的整体生存呈正相关。CCL7缺乏会损害cDC1在TME中的浸润以及CD8 ⁺和CD4 ⁺的随后扩展支气管引流淋巴结和TME中的T细胞，从而促进了KP小鼠模型中的肿瘤发展。单独或与抗PD-1组合使用CCL7进入肺部可显着抑制肿瘤的发展，并延长KP和KL小鼠的生存期。这些发现表明，CCL7可能作为非小细胞肺癌检查点免疫疗法的生物标志物和佐剂。