决定异体 CAR T 细胞排斥与扩增的细胞和分子机制
Cellular and molecular mechanisms determining allogeneic CAR T cell rejection and expansion.
我们评估了11例接受单一批次cemacabtagene ansegedleucel(cema-cel)治疗的大B细胞淋巴瘤患者,cemacabtagene ansegedleucel是一种异体抗CD19 CAR T产品。
英文原题:Current progress in the elucidation of Acute Myeloid Leukemia (AML) immune landscapes.
免疫逃逸是癌症的一个关键标志,因为围绕这一主题的机制仍有待完全阐明。
免疫逃逸是癌症的一个关键标志,因为围绕这一主题的机制仍有待完全阐明。在急性髓系白血病(AML)中,免疫逃逸在使疾病逃避宿主免疫系统方面发挥着关键作用。该疾病的异质性进一步使治疗复杂化,因为这影响了参与免疫调节的若干关键组成部分,从而导致AML进展。肿瘤微环境(TME)可能受到AML的影响,因为骨髓成分可能被劫持。此外,AML调节表面标志物表达,这使诸如造血干细胞同种移植或依赖T细胞功能的CAR T细胞治疗等治疗复杂化。在此,我们讨论AML免疫景观的当前进展,包括当前疗法和可能作为未来治疗开发潜在靶点的免疫标志物。我们还提出若干前景,包括利用基因编辑技术提高CAR治疗的疗效,以及使用免疫检查点抑制剂,这可能有助于造血干细胞同种移植和CAR治疗。
Immune evasion is a pivotal hallmark of cancer as mechanisms revolving around this subject remain to be fully elucidated. In acute myeloid leukemia (AML), immune evasion plays a critical role in masking the disease from the host immune system. The heterogenous nature of this disease further complicates treatment as this affects several crucial components involved in immune regulation which resulted in AML progression. The tumor microenvironment (TME) could be influenced by AML as the bone marrow components could be hijacked. Moreover, AML modulates surface marker expression, this complicates treatment such as hematopoietic stem cell allograft or CAR T-cell therapy which depends on T-cell functionality. Here, we discuss the current development in AML immune landscapes which includes current therapies and immune markers which could potentially serve as possible targets for development of future therapy. We also suggest several prospects by using gene editing technology to improve the efficacy of CAR therapy and the use of immune checkpoint inhibitors which could aid in hematopoietic stem cell allograft and CAR therapy.
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