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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >IL-7 induces bone loss in vivo by induction of receptor activator of nuclear factor kappa B ligand and tumor necrosis factor a from T cells
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IL-7 induces bone loss in vivo by induction of receptor activator of nuclear factor kappa B ligand and tumor necrosis factor a from T cells

机译：IL-7通过诱导T细胞核因子κB配体和肿瘤坏死因子a的受体激活剂诱导体内骨丢失

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IL-7, a powerful lymphopoietic cytokine, is elevated in rheumatoid arthritis (RA) and known to induce bone loss when administered in vivo. IL-7 has been suggested to induce bone loss, in part, by stimulating the proliferation of B220(+) cells, a population capable of acting as early osteoclast (OC) precursors. However, the mechanism by which IL-7 leads to differentiation of precursors into mature OCs remains unknown. We previously reported that, in vitro, IL-7 up-regulated T cell cytokines including receptor activator of nuclear factor kappaB ligand (RANKL). To demonstrate the importance of T cells to the bone-wasting effect of IL-7 in vivo, we have now examined IL-7-induced bone loss in T cell-deficient nude mice. We show that T cell-replete mice undergo significant osteoclastic bone loss after IL-7 administration, concurrent with induction of RANKL and tumor necrosis factor alpha (TNF-alpha) secretion by splenic T cells. In contrast, nude mice were resistant to IL-7-induced bone loss and showed no detectable increase in either RANKL or TNF-alpha, despite an up-regulation of B220+ cells. Importantly, T cell adoptive transfer into nude mice restored IL-7-induced bone loss, and RANKL and TNF-alpha secretion, demonstrating that T cells are essential mediators of IL-7-induced bone loss in vivo. [References: 26]
机译：IL-7是一种强大的淋巴细胞细胞因子，在类风湿关节炎（RA）中升高，并且在体内给药时会引起骨质流失。有人提出IL-7会部分地通过刺激B220（+）细胞的增殖来诱导骨丢失，B220（+）细胞能够充当早期破骨细胞（OC）的前体。但是，IL-7导致前体分化为成熟OC的机制仍然未知。我们先前曾报道过，在体外，IL-7上调了T细胞细胞因子，包括核因子kappaB配体的受体激活剂（RANKL）。为了证明T细胞对体内IL-7的骨浪费作用的重要性，我们现在检查了T细胞缺陷裸鼠中IL-7诱导的骨丢失。我们显示，T细胞充足的小鼠在IL-7给药后会发生明显的破骨性骨丢失，并伴随脾脏T细胞诱导RANKL和肿瘤坏死因子α（TNF-α）分泌。相比之下，尽管B220 +细胞上调，但裸鼠对IL-7诱导的骨丢失有抵抗力，并且RANKL或TNF-α均未显示可检测的增加。重要的是，过继转移到裸鼠中的T细胞恢复了IL-7诱导的骨丢失以及RANKL和TNF-α的分泌，这表明T细胞是体内IL-7诱导的骨丢失的重要介质。 [参考：26]

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