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细胞巨乳病毒通过骨髓衍生的内皮原生细胞导致移植功能不佳

Weiran Lv^1,2, Ya Zhou², Ke Zhao²

¹Department of Hematologic Oncology, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, China.

Frontiers in microbiology

|October 3, 2024

概括

人类细胞巨型病毒 (HCMV) 感染会损害骨髓内皮原生细胞 (BM-EPCs),导致干细胞移植后的移植功能不佳. HCMV通过VDR和p38 MAPK增加TGF-β1,阻碍了造血和移植的恢复.

科学领域:

干细胞移植干细胞移植
病毒学病毒学
免疫学免疫学免疫学

背景情况:

缺陷的移植功能 (PGF) 是全源造血干细胞移植 (allo-HSCT) 的一个主要并发症.
人类细胞巨核病毒 (HCMV) 是已知的PGF风险因素,但其潜在机制尚未完全理解.
骨髓内皮原生细胞 (BM-EPCs) 对血液形成至关重要,它们的功能障碍有助于PGF.

研究的目的:

研究HCMV对BM-EPC功能的影响.
阐明HCMV影响BM-EPCs并导致PGF的分子机制.

主要方法:

在体外检查了HCMV病毒性患者的PGF和HCMV感染的BM-EPCs的BM-EPC.
评估了细胞增殖,管形成,迁移,造血支持,细胞亡和TGF-β1分泌.
研究了维生素D受体 (VDR) 和p38 MAPK通路的作用.

主要成果:

冠状病毒感染损害了BM-EPC的功能,减少了增殖,管形成,迁移和造血支持,同时增加了细胞亡和TGF-β1分泌.
由BM-EPCs引起的HCMV诱导的TGF-β1分泌在体外显著抑制了血液形成.
HCMV降低了VDR的调节,激活了p38 MAPK通路,从而促进了TGF-β1分泌.

结论:

HCMV感染BM-EPCs,导致功能障碍,并通过依赖VDR的p38 MAPK激活通路增强TGF-β1分泌.
这种HCMV诱导的BM-EPC功能障碍损害了造血原体的支持,导致allo-HSCT后的PGF病变.
针对这一机制为PGF提供了潜在的治疗策略.

关键词:

体前代细胞是内皮前代细胞.人类细胞巨型病毒糟糕的移植功能移植功能不佳转化增长因子β转化增长因子β.维生素D受体是维生素D的受体.

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