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

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。

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(ONFH).After the bone injured,Treg cells homed to the injured area by CCL22/CCR4 axis pathway and were activated to syntheses for tissue repair by promoting factors of STAT5/FoxP3 pathway with BMSCs to regulate osteogenesis and angiogenesis to promote bone repair.The MiR-155/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.