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TIM3 在骨髓增生异常综合征中的研究进展

英文原题:Advances in the study of TIM3 in myelodysplastic syndrome.

PubMed 2025/08/19(内容时间) Front Immunol Q1 · IF 7(JCR 2025)

研究概要

骨髓增生异常综合征(MDS)是起源于造血干细胞的异质性髓系克隆性疾病。

中文摘要

骨髓增生异常综合征(MDS)是起源于造血干细胞的异质性髓系克隆性疾病。MDS的发病率(中国1.51/100,000,欧美4-5/100,000)高于任何类型的白血病。近年来,免疫调节失衡和肿瘤微环境紊乱在MDS发病机制中受到越来越多的关注。T细胞免疫球蛋白和黏蛋白结构域蛋白3(TIM-3)是一种重要的抑制性免疫检查点分子,广泛表达于T细胞、NK细胞、树突状细胞、单核/巨噬细胞等免疫细胞。大量研究证实,TIM-3在多种实体瘤和血液肿瘤中异常表达,在调控肿瘤逃逸和免疫耗竭中发挥重要作用。本文重点综述TIM-3在MDS中的相关研究,并总结本团队在该领域的研究发现。同时结合最新临床试验,探讨TIM-3在MDS诊断和治疗中的潜在应用。阻断TIM-3在MDS疾病进展中具有“靶向抑制肿瘤细胞”和“重塑免疫功能”的双重作用,为MDS患者提供了新的治疗策略和希望。

展开英文摘要原文

Myelodysplastic syndromes (MDS) are heterogeneous myeloid clonal disorders derived from hematopoietic stem cells. The incidence of MDS (1.51/100,000 in China, 4-5/100,000 in Europe and America) is higher than any subtype of leukemia. In recent years, the imbalance of immune regulation and tumor microenvironmental disorders have received increasing attention in the pathogenesis of MDS. T-cell immunoglobulin and mucin-domain containing protein 3 (TIM-3) is an important inhibitory immune checkpoint molecule, widely expressed in T cells, NK cells, and dendritic cells, monocytes/macrophages and other immune cells. Numerous studies have confirmed that TIM-3 is aberrantly expressed in a variety of solid and hematologic tumors and plays an important role in regulating tumor escape and immune depletion. In this paper, we focus on reviewing the relevant studies of TIM-3 in MDS and summarize the findings of our team in this field. We also discuss the potential application of TIM-3 in the diagnosis and treatment of MDS in conjunction with the latest clinical trials. Blocking TIM-3 has both 'tumor cell-targeted inhibition' and 'immune function remodeling' dual roles in MDS disease progression, which provides new therapeutic strategies and hope for MDS patients.

论文信息

作者
Guo X、Yu S、Tao J、Wang Y、Shao Z、Fu R、Li L
单位
Department of Hematology, Tianjin Medical University General Hospital, Tianjin, China.China
文献类型
综述
期刊
Frontiers in immunology2025
原文标识
PubMed 40904469 · DOI 10.3389/fimmu.2025.1647401