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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The immune regulatory protein B7-H3 promotes osteoblast differentiation and bone mineralization.
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The immune regulatory protein B7-H3 promotes osteoblast differentiation and bone mineralization.

机译：免疫调节蛋白B7-H3促进成骨细胞分化和骨矿化。

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B7-H3, a member of the B7 family of the Ig superfamily proteins, is expressed on the surface of the antigen-presenting cells and down-regulates T cell functions by engaging an unknown counterreceptor on T cells. Although B7-H3 is ubiquitously expressed, its potential nonimmune functions have not been addressed. We found that B7-H3 is highly expressed in developing bones during embryogenesis and that its expression increases as osteoblast precursor cells differentiate into mature osteoblasts. In vitro bone formation by osteoblastic cells was inhibited when B7-H3 function was interrupted by the soluble recombinant protein B7-H3-Fc. Analysis of calvarial cells derived from neonatal B7-H3 knockout (KO) mice revealed normal numbers of osteoblast precursor cells possessing a normal proliferative capacity. However, the B7-H3-deficient calvarial cells exhibited impaired osteogenic differentiation, resulting in decreased mineralized bone formation in vitro. These results suggest that B7-H3 is required for the later phase of osteoblast differentiation. Although B7-H3 KO mice had no gross skeletal abnormalities, they displayed a lower bone mineral density in cortical (but not trabecular) bones compared with WT controls. Consistent with the reduced bone mineral density, the femurs of B7-H3 KO mice were more susceptible to bone fracture compared with those of WT mice. Taken together, these results indicate that B7-H3 and its unknown counterreceptor play a positive regulatory role in bone formation. In addition, our findings identified B7-H3 as another molecule that has a dual role in the bone-immune interface.
机译：B7-H3是Ig超家族蛋白B7家族的成员，在抗原呈递细胞的表面表达，并通过在T细胞上结合未知的反受体来下调T细胞的功能。尽管普遍表达B7-H3，但尚未解决其潜在的非免疫功能。我们发现B7-H3在胚胎发育过程中在发育中的骨中高表达，并且随着成骨细胞前体细胞分化为成熟成骨细胞，其表达增加。当可溶性重组蛋白B7-H3-Fc中断B7-H3功能时，成骨细胞的体外骨形成受到抑制。分析来自新生B7-H3基因敲除（KO）小鼠的颅盖骨细胞，发现正常数目的成骨细胞前体细胞具有正常的增殖能力。但是，缺乏B7-H3的颅盖细胞表现出成骨分化受损，导致体外矿化骨形成减少。这些结果表明，成骨细胞分化的后期需要B7-H3。尽管B7-H3 KO小鼠没有明显的骨骼异常，但与WT对照相比，它们在皮质（而非小梁）骨中显示出较低的骨矿物质密度。与降低的骨矿物质密度一致，与WT小鼠相比，B7-H3 KO小鼠的股骨更容易发生骨折。综上所述，这些结果表明B7-H3及其未知的反受体在骨形成中起着积极的调节作用。此外，我们的发现确定B7-H3是在骨免疫界面中具有双重作用的另一种分子。

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