Inter- and intracellular signaling in secondary osteoporosis
Inter- and intracellular signaling in secondary osteoporosis
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DOI：
10.1007/s007740300010
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发表时间：
2003
影响因子：
3.3
通讯作者：
Yoshiya Tanaka;Y. Okada;Toshitaka Nakamura
中科院分区：
文献类型：
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作者：
Yoshiya Tanaka;Y. Okada;Toshitaka Nakamura
在这方面，我们首先提出趋化因子巨噬细胞炎性蛋白（MIP）-1α和MIP-1通过“由内而外的信号传导”触发T细胞整合素功能[11-15]。术语“趋化因子”最初指定为趋化性细胞因子，该术语现在包括50多种细胞因子，如MIP-1α、MIP-1、白细胞介素（IL）-8和单核细胞趋化蛋白（MCP）-1。趋化因子由发炎组织中活化的巨噬细胞和淋巴细胞大量产生，它们触发白细胞上的整合素并诱导趋化性，导致白细胞在那里积聚。我们还观察到，趋化因子MIP-1α和MCP-1不仅诱导趋化性，
In this regard, we first proposed that the chemokines, macrophage inflammatory protein (MIP)-1α and MIP-1 trigger T-cell integrin functions through “insideto-out signaling”[11–15]. The term “chemokine” originally designated a chemotactic cytokine, and this term now includes more than 50 cytokines, such as MIP-1α, MIP-1, interleukin (IL)-8, and monocyte chemotactic protein (MCP)-1. Chemokines are produced in large amounts from activated macrophages and lymphocytes in inflamed tissue, and they trigger integrins on leukocytes and induce chemotaxis, resulting in leukocyte accumulation there. We also observed that the chemokines MIP-1α and MCP-1 induce not only chemotaxis of