CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Tumor infiltrating B lymphocytes (TIBs) associate with poor clinical outcomes, unfavorable therapeutic benefit and immunosuppressive context in metastatic clear cell renal cell carcinoma (mccRCC) patients treated with anti-PD-1 antibody plus Axitinib.
Tumor infiltrating B lymphocytes (TIBs) associate with poor clinical outcomes, unfavorable therapeutic benefit and immunosuppressive context in metastatic clear cell renal cell carcinoma (mccRCC) patients treated with anti-PD-1 antibody plus Axitinib.
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我们的研究揭示，TIBs 浸润预示接受抗 PD-1 抗体联合阿昔替尼治疗的 mccRCC 患者不良结局。作为必然结果，TIBs 与 M2 巨噬细胞和 Tregs 正相关，导致随后多个免疫检查点相关的 T 细胞耗竭。因此，在高 TIBs 的 mccRCC 患者中，仅阻断 PD-1 不足以有效逆转 T 细胞耗竭。
免疫检查点抑制剂（ICIs）联合酪氨酸激酶抑制剂（TKIs）已成为转移性肾细胞癌患者的一线治疗。本研究旨在探讨肿瘤浸润B淋巴细胞（TIBs）对联合治疗的影响。
对2020年3月至2023年6月期间接受抗PD-1抗体联合阿昔替尼治疗的115例转移性透明细胞肾细胞癌（mccRCC）患者的临床记录进行了回顾性分析。观察指标：客观缓解率（ORR）、总生存期（OS）、无进展生存期（PFS）及免疫特征。
高TIBs的患者联合治疗的ORR较低（p = 0.033）。在接受联合治疗的mccRCC患者中，TIBs是较差OS（p = 0.013）和PFS（p = 0.021）的独立预测因素。TIBs浸润与更多的CD4 + T（p < 0.001）、CD8 + T（p < 0.001）、M2巨噬细胞（p = 0.020）和调节性T细胞（Tregs）（p = 0.004）相关。在TIBs高的患者中，CD4 + T细胞中PD-1、CTLA-4和TIM-3阳性率显著升高（分别为p = 0.038、0.029和0.002），CD8 + T细胞中亦显著升高（分别为p = 0.006、0.026和< 0.001）。
Immune checkpoint inhibitors (ICIs) plus tyrosine kinase inhibitors (TKIs) has become first-line therapy for metastatic renal cell carcinoma patients. This study aims to investigate the effect of tumor infiltrating B lymphocytes (TIBs) on the combination therapy.
The retrospective analysis was conducted on the clinical records of 115 metastatic clear cell renal cell carcinoma (mccRCC) patients treated with anti-PD-1 antibody plus Axitinib between March 2020 and June 2023. Observation target: objective response rate (ORR), and overall survival (OS), progression-free survival (PFS) and immune profile.
Patients with high TIBs portended lower ORR of the combination therapy (p = 0.033). TIBs was an independent predictor for poorer OS (p = 0.013) and PFS (p = 0.021) in mccRCC patients with combination treatment. TIBs infiltration was associated with more CD4 + T (p < 0.001), CD8 + T (p < 0.001), M2 macrophages (p = 0.020) and regulatory T cells (Tregs) (p = 0.004). In TIBs high patients, the percentages of PD-1, CTLA-4 and TIM-3 positive rate were significantly increased in CD4 + T (p = 0.038, 0.029 and 0.002 respectively) and CD8 + T cells (p = 0.006, 0.026 and < 0.001 respectively).
Our study revealed TIBs infiltration predicted adverse outcomes in mccRCC patients treated with anti-PD-1 antibody plus Axitinib. As a corollary, TIBs positively associated with M 2 macrophages and Tregs, leading to subsequent multiple immune checkpoints related exhaustion of T cells. Thus, only PD-1 blockade are inadequate to reverse T cells exhaustion effectively in high TIBs mccRCC patients.
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