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白细胞介素-7调节实体瘤患者的破骨细胞生成。

IL-7 modulates osteoclastogenesis in patients affected by solid tumors.

作者信息

Roato Ilaria, Gorassini Eva, Brunetti Giacomina, Grano Maria, Ciuffreda Libero, Mussa Antonio, Ferracini Riccardo

机构信息

Center for Experimental Research and Medical Studies, University and A.S.O. San Giovanni Battista, Turin, Italy.

出版信息

Ann N Y Acad Sci. 2007 Nov;1117:377-84. doi: 10.1196/annals.1402.002. Epub 2007 Jun 21.

Abstract

High levels of interleukin-7 (IL-7) have been associated with bone loss due to its stimulatory osteoclastogenic activity. Osteolytic patients' peripheral blood mononuclear cells (PBMCs) differentiate into osteoclasts without adding stimulating factors. Now, we investigated the potential role of IL-7 in the spontaneous osteoclastogenesis occurring in these patients. We identified significant differences in serum IL-7 levels between patients with/without bone metastases, suggesting that IL-7 might be effective as a clinical marker of disease progression. In patients' PBMC cultures we demonstrated that IL-7 stimulates osteoclastogenesis by inducing TNF-alpha release by T and B cells. These findings add further details to the disclosure of the mechanisms controlling bone metastases in solid tumors.

摘要

高水平的白细胞介素-7(IL-7)因其刺激破骨细胞生成的活性而与骨质流失有关。溶骨性患者的外周血单个核细胞(PBMCs)在不添加刺激因子的情况下可分化为破骨细胞。现在,我们研究了IL-7在这些患者发生的自发性破骨细胞生成中的潜在作用。我们发现有/无骨转移患者的血清IL-7水平存在显著差异,这表明IL-7可能作为疾病进展的临床标志物有效。在患者的PBMC培养物中,我们证明IL-7通过诱导T细胞和B细胞释放肿瘤坏死因子-α来刺激破骨细胞生成。这些发现为实体瘤中控制骨转移机制的揭示增添了更多细节。

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