髓源性抑制细胞在骨髓增生异常综合征中的研究进展

骨髓增生异常综合征(MDS)以造血细胞发育异常和无效造血为特征,骨髓造血微环境内髓源性抑制细胞(MDSC)的异常扩增和激活可能是重要原因。MDSC细胞扩增与激活导致自然杀伤细胞、CD8+T细胞功能低下与耗竭,并募集炎症细胞及因子,导致MDS患者遗传异常的进一步积累,致使MDS疾病进展。肿瘤环境炎症因子的积累诱导程序性死亡受体1(PD-1)在造血干、祖细胞上的表达和MDSC细胞程序性死亡受体配体1(PD-L1)过表达,PD-1/PD-L1的相互作用导致MDS造血祖细胞的凋亡和无效造血。靶向MDSC的试验及临床研究证实,纠正或逆转MDS免疫失调的骨髓微环境是恢复有效造血功能的治疗策略。

Progress of myeloid-derived suppressor cells in myelodysplastic syndrome

Myelodysplastic syndrome (MDS) is characterized by dysplastic and ineffective hematopoiesis that can result from aberrant expansion and activation of myeloid-derived suppressor cells (MDSC) within the bone marrow microenvironment. The proliferation and activation of MDSC lead to the dysfunction and depletion of natural killer cells and CD8 + T cells, and the recruitment of inflammatory cells and factors leads to the further accumulation of genetic abnormalities in MDS patients, leading to the progression of MDS. The accumulation of inflammatory cytokines in the tumor environment induces the expression of programmed death receptor 1 (PD-1) in hematopoietic stem cells and hematopoietic progenitor cells and the overexpression of programmed death receptor ligand 1 (PD-L1) in MDSC, and the interaction of PD-1/PD-L1 leads to the apoptosis of MDS hematopoietic progenitor cells and ineffective hematopoiesis. The experiments and clinical studies targeting MDSC have confirmed that correcting or reversing the bone marrow microenvironment of immune disorders in MDS is a therapeutic strategy to restore effective hematopoietic function.