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从免疫失调到骨髓增生异常综合征的治疗前景:综述

From Immune Dysregulations to Therapeutic Perspectives in Myelodysplastic Syndromes: A Review.

作者信息

Comont Thibault, Treiner Emmanuel, Vergez François

机构信息

Department of Internal Medicine, IUCT-Oncopole, Toulouse University Hospital (CHU-Toulouse), 31300 Toulouse, France.

Cancer Research Center of Toulouse, Unité Mixte de Recherche (UMR) 1037 INSERM, ERL5294 Centre National de La Recherche Scientifique, 31100 Toulouse, France.

出版信息

Diagnostics (Basel). 2021 Oct 26;11(11):1982. doi: 10.3390/diagnostics11111982.

DOI:10.3390/diagnostics11111982
PMID:34829329
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8620222/
Abstract

The pathophysiology of myelodysplastic syndromes (MDSs) is complex and often includes immune dysregulation of both the innate and adaptive immune systems. Whereas clonal selection mainly involves smoldering inflammation, a cellular immunity dysfunction leads to increased apoptosis and blast proliferation. Addressing immune dysregulations in MDS is a recent concept that has allowed the identification of new therapeutic targets. Several approaches targeting the different actors of the immune system have therefore been developed. However, the results are very heterogeneous, indicating the need to improve our understanding of the disease and interactions between chronic inflammation, adaptive dysfunction, and somatic mutations. This review highlights current knowledge of the role of immune dysregulation in MDS pathophysiology and the field of new drugs.

摘要

骨髓增生异常综合征(MDS)的病理生理学很复杂,通常包括先天性和适应性免疫系统的免疫失调。虽然克隆选择主要涉及隐匿性炎症,但细胞免疫功能障碍会导致细胞凋亡增加和原始细胞增殖。解决MDS中的免疫失调是一个新的概念,它使我们能够识别新的治疗靶点。因此,已经开发了几种针对免疫系统不同作用因素的方法。然而,结果差异很大,这表明有必要加深我们对该疾病以及慢性炎症、适应性功能障碍和体细胞突变之间相互作用的理解。这篇综述重点介绍了目前关于免疫失调在MDS病理生理学中的作用以及新药领域的知识。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f18/8620222/9a7f8401778b/diagnostics-11-01982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f18/8620222/9a7f8401778b/diagnostics-11-01982-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f18/8620222/9a7f8401778b/diagnostics-11-01982-g001.jpg

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