Unveiling T cell evasion mechanisms to immune checkpoint inhibitors in acute myeloid leukemia  

作　　者：Lindsay Gurska Kira Gritsman 

机构地区：[1]Department of Cell Biology,Albert Einstein College of Medicine,Bronx,NY 10461,USA [2]Department of Medical Oncology,Montefiore Medical Center,Albert Einstein College of Medicine,Bronx,NY 10461,USA

出　　处：《Cancer Drug Resistance》2023年第3期674-687,共14页癌症耐药（英文）

基　　金：supported by the National Institutes of Health(NIH)Grants R01CA196973(Gritsman K)and F31CA247172(Gurska L).

摘　　要：Acute myeloid leukemia (AML) is a heterogeneous and aggressive hematologic malignancy that is associated with a high relapse rate and poor prognosis. Despite advances in immunotherapies in solid tumors and other hematologic malignancies, AML has been particularly difficult to treat with immunotherapies, as their efficacy is limited by the ability of leukemic cells to evade T cell recognition. In this review, we discuss the common mechanisms of T cell evasion in AML: (1) increased expression of immune checkpoint molecules;(2) downregulation of antigen presentation molecules;(3) induction of T cell exhaustion;and (4) creation of an immunosuppressive environment through the increased frequency of regulatory T cells. We also review the clinical investigation of immune checkpoint inhibitors (ICIs) in AML. We discuss the limitations of ICIs, particularly in the context of T cell evasion mechanisms in AML, and we describe emerging strategies to overcome T cell evasion, including combination therapies. Finally, we provide an outlook on the future directions of immunotherapy research in AML, highlighting the need for a more comprehensive understanding of the complex interplay between AML cells and the immune system.

关 键 词：Acute myeloid leukemia T cells immune checkpoint immune evasion 

分 类 号：R733.71[医药卫生—肿瘤]