肿瘤细胞治疗研究
英文原题：Elotuzumab enhances the anti-tumor activity of Vγ9Vδ2 T cells against primary effusion lymphoma.
我们的发现首次证明，Elo可直接增强γδ T细胞对PEL的抗肿瘤活性，为将Elo与γδ T细胞疗法联合作为这种难治性淋巴瘤的潜在治疗策略提供了新的临床前证据。
原发性渗出性淋巴瘤（PEL）是一种侵袭性B细胞淋巴瘤，目前尚无标准治疗方案。Vγ9Vδ2 T细胞有助于清除肿瘤，但其自身细胞毒性有限。Elotuzumab（Elo）是一种获批用于多发性骨髓瘤的抗SLAMF7单克隆抗体，主要通过NK细胞发挥作用；然而，其对γδ T细胞的直接作用尚未见报道。在本研究中，我们探讨了Elo是否能增强γδ T细胞对PEL的细胞毒性。我们发现SLAMF7在PEL细胞和γδ T细胞上均有表达。Elo处理显著增加了γδ T细胞的细胞毒性和脱颗粒，而这些效应可被Fc受体阻断或Fc缺陷型Elo所阻止，表明其机制为抗体依赖性细胞介导的细胞毒性（ADCC）。我们的研究结果首次证明，Elo可直接增强γδ T细胞对PEL的抗肿瘤活性，为将Elo与γδ T细胞疗法联合作为这种难治性淋巴瘤的潜在治疗策略提供了新的临床前证据。
Primary Effusion Lymphoma (PEL) is an aggressive B-cell lymphoma with no standard treatment. Vγ9Vδ2 T cells contribute to tumor eradication but have limited cytotoxicity on their own. Elotuzumab (Elo), an anti-SLAMF7 monoclonal antibody approved for multiple myeloma, primarily acts through NK cells; however, its direct effect on γδ T cells has not been reported. In this study, we examined whether Elo enhances γδ T cell cytotoxicity against PEL. We found that SLAMF7 is expressed on both PEL cells and γδ T cells. Elo treatment significantly increased γδ T cell cytotoxicity and degranulation, and these effects were prevented by Fc receptor blockade or by Fc-deficient Elo, indicating an antibody-dependent cellular cytotoxicity (ADCC) mechanism. Our findings demonstrate for the first time that Elo directly boosts γδ T cell anti-tumor activity against PEL, offering novel preclinical evidence for combining Elo with γδ T cell therapy as a potential treatment strategy for this intractable lymphoma.
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