骨免疫调控成骨在激素性股骨头坏死的作用△

Role of bone immunoregulation osteogenesis in glucocorticoid-induced osteonecrosis of femoral head

摘要:

骨免疫调控成骨是骨修复领域研究的热点，调节性 T 细胞（regulatory T cells, Treg）是介导骨免疫成骨的核心细胞且与激素诱发 ONFH 密切相关。骨损伤后 Treg 细胞经 CCL22/CCR4 轴调控定向归巢至损伤局部并经 STAT5/FoxP3 通路激活合成促组织修复因子，并与 BMSCs 串话调控成骨成血管促进骨修复。MiR-155/SOCS1 调节回路调控 STAT5/FoxP3 通路的激活，激素抑制 MiR-155，促进 SOCS1 表达抑制 STAT5/FoxP3 通路与 Treg 细胞激活。调控 Treg 细胞定向归巢，MiR-155 靶向转染 T 细胞抑制 SOCS1 表达，激活 STAT5/FoxP3 通路与 Treg 细胞，协同构建由 Treg 细胞介导的骨免疫调控成骨微环境，调控 BMSCs 成骨成血管修复骨坏死，从骨免疫研究激素性 ONFH 发病机制和防治是新思路。

Abstract:

Bone-immunoregulation osteogenesis is a hot topic in the research field of bone repair. The regulatory T cell (Treg) is the core cell mediating -immunoregulation osteogenesis, which is closely related to glucocorticoid-induced osteonecrosis of femoral head (ON- FH). After the bone injured, Treg cells homed to the injured area by CCL22/CCR4 axis pathway and were activated to syntheses for tissue re- pair by promoting factors of STAT5/FoxP3 pathway with BMSCs to regulate osteogenesis and angiogenesis to promote bone repair. The MiR155/SOCS1 regulatory circuit regulates the activation of STAT5/FoxP3 pathway, whereas the glucocorticoid inhibits MiR- 155, promotes SOCS1 expression and inhibits the activation of STAT5/FoxP3 pathway and Treg cells. Targeted homing of Treg cells and MiR-155 targeted transfection in T cells to inhibit SOCS1 expression, while activate STAT5/FoxP3 pathway and Treg cells, as well as bone immunoregulation of osteogenic microenvironment mediated by Treg cells, and regulation of BMSCs-osteoblast angiogenesis and osteonecrosis might be a new approach to study the pathogenesis and prevention of glucocorticoid-induced ONFH.