{"title":"针对小胶质细胞中的 TAK1 治疗 CAR T 细胞神经毒性。","authors":"","doi":"10.1038/s43018-024-00765-6","DOIUrl":null,"url":null,"abstract":"We profiled microglia using single-cell multi-omics techniques in lymphoma-bearing mice and patients who developed neurotoxicity after CAR19 T cell transfer. We discovered that microglial activation after CAR19 T cell infusion was mediated mainly by the kinase TAK1, which suggests that targeting TAK1 in patients receiving CAR19 T cell-based cancer immunotherapy could treat neurotoxicity.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":"5 8","pages":"1143-1144"},"PeriodicalIF":23.5000,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Targeting TAK1 in microglia to treat CAR T cell neurotoxicity\",\"authors\":\"\",\"doi\":\"10.1038/s43018-024-00765-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We profiled microglia using single-cell multi-omics techniques in lymphoma-bearing mice and patients who developed neurotoxicity after CAR19 T cell transfer. We discovered that microglial activation after CAR19 T cell infusion was mediated mainly by the kinase TAK1, which suggests that targeting TAK1 in patients receiving CAR19 T cell-based cancer immunotherapy could treat neurotoxicity.\",\"PeriodicalId\":18885,\"journal\":{\"name\":\"Nature cancer\",\"volume\":\"5 8\",\"pages\":\"1143-1144\"},\"PeriodicalIF\":23.5000,\"publicationDate\":\"2024-05-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature cancer\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.nature.com/articles/s43018-024-00765-6\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cancer","FirstCategoryId":"3","ListUrlMain":"https://www.nature.com/articles/s43018-024-00765-6","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
我们利用单细胞多组学技术对淋巴瘤小鼠和接受 CAR19 T 细胞转移后出现神经毒性的患者的小胶质细胞进行了分析。我们发现,CAR19 T 细胞输注后的小胶质细胞活化主要由激酶 TAK1 介导,这表明在接受基于 CAR19 T 细胞的癌症免疫疗法的患者中靶向 TAK1 可以治疗神经毒性。
Targeting TAK1 in microglia to treat CAR T cell neurotoxicity
We profiled microglia using single-cell multi-omics techniques in lymphoma-bearing mice and patients who developed neurotoxicity after CAR19 T cell transfer. We discovered that microglial activation after CAR19 T cell infusion was mediated mainly by the kinase TAK1, which suggests that targeting TAK1 in patients receiving CAR19 T cell-based cancer immunotherapy could treat neurotoxicity.
期刊介绍:
Cancer is a devastating disease responsible for millions of deaths worldwide. However, many of these deaths could be prevented with improved prevention and treatment strategies. To achieve this, it is crucial to focus on accurate diagnosis, effective treatment methods, and understanding the socioeconomic factors that influence cancer rates.
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