期刊
DIAGNOSTICS
卷 11, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/diagnostics11111982
关键词
myelodysplastic syndromes; immune; inflammation; T-cell
The pathophysiology of MDS involves immune dysregulation of both innate and adaptive immune systems, leading to increased apoptosis and blast proliferation. Targeting immune dysregulations has identified new therapeutic targets, but results are heterogeneous, indicating a need for a better understanding of the disease and interactions between chronic inflammation, adaptive dysfunction, and somatic mutations.
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.
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