免疫与炎症对破骨细胞分化的影响

Effects of immunity and inflammation on osteoclast differentiation

破骨细胞是骨吸收细胞,来源于造血前体细胞,需巨噬细胞集落核因子κB(NF-κB)的刺激因子和受体激活剂配体(RANKL)才能生存、增殖、分化和激活。RANKL与其受体RANK的结合触发破骨细胞前体分化为破骨细胞。目前,可以明确的是破骨细胞和免疫细胞是受到共同调控的,破骨细胞和免疫细胞不仅有着共同的祖细胞,而且还有着许多共同调节因子,如NF-κB配体的受体激活剂,肿瘤坏死因子α(TNF-α)和干扰素γ(IFN-γ)。因此,炎症情况下所产生的一系列免疫细胞、细胞因子以及酶对破骨细胞的分化都会产生多且复杂的影响。在炎症情况下,RANKLRANK-骨保护素(OPG)系统会受到较多影响。全文综述免疫与炎症及在炎症情况下RANKL-RANK-OPG系统调控破骨细胞分化的研究进展。

Osteoclasts are bone-resorbing cells derived from hematopoietic precursor cells which require macrophage colony-stimulating factor of nuclear factor kappa B(NF-κB)and receptor activator of NF-κB ligand(RANKL)for survival,proliferation,differentiation,and activation.Binding of RANKL to its receptor activator of NF-κB(RANK),triggers osteoclast precursor’s differentiation into osteoclasts.At present,it is now clear that osteoclasts and immune cells are co-regulated,and they not only share common progenitor cells,but also have many co-regulators,such as RANKL,tumor necrosis factorα(TNF-α)and interferonγ(IFN-γ).Therefore,a series of immune cells,cytokines and enzymes produced under inflammatory conditions have massive and complex effects on the differentiation of osteoclasts.In the case of inflammation,the RANKL-RANK-OPG system is more affected.This article reviews the research progress of immune and inflammation,and the regulation of osteoclast differentiation by RANKL-RANK-OPG system under the condition of inflammation.