肿瘤细胞治疗研究
英文原题：A CD38/CD3xCD28 trispecific T-cell engager as a potentially active agent in multiple myeloma patients relapsed and/or refractory to anti-CD38 monoclonal antibodies.
越来越多的证据表明，在复发/难治性多发性骨髓瘤（RRMM）患者接受T细胞重定向治疗后，会出现BCMA和GPRC5D丢失。
在复发/难治性多发性骨髓瘤（RRMM）患者接受T细胞重定向治疗后，BCMA和GPRC5D丢失的证据日益增多。虽然抗CD38单克隆抗体（mAb）治疗后复发时未观察到CD38完全丢失，但存在表面CD38表达下调和NK细胞数量及功能下降，这使得这些患者对再次使用抗CD38 mAb治疗产生耐药。在此，我们提供临床前证据表明，既往暴露于抗CD38 mAb的RRMM患者可能受益于对CD38抗原密度和NK细胞活性依赖较少的T细胞免疫疗法，例如新型CD38/CD3xCD28三特异性T细胞衔接器SAR442257。
There is accumulating evidence of BCMA and GPRC5D loss after treatment with T-cell redirecting therapies in patients with relapsed/refractory multiple myeloma (RRMM). While complete CD38 loss is not observed upon relapses after treatment with anti-CD38 monoclonal antibodies (mAb), there is downregulation of surface CD38 expression and decreased number and function of NK cells, which renders these patients resistant to retreatment with anti-CD38 mAb. Here, we provide preclinical evidence that RRMM patients previously exposed to anti-CD38 mAb could benefit from T-cell-based immunotherapy that depend less on CD38 antigen density and NK-cell activity, such as the novel CD38/CD3xCD28 trispecific T-cell engager, SAR442257.
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