IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo.
IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo.
复制标题
IP-10，A -C-X-C-趋化因子，在体内引起有效的胸腺依赖性抗肿瘤反应。
DOI：
10.1084/jem.178.3.1057
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发表时间：
1993-09-01
影响因子：
15.3
通讯作者：
Leder, P
中科院分区：
文献类型：
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作者：
Luster, A D;Leder, P
IP-10是促炎症细胞因子-C-X-C-趋化因子超家族的一员，其分泌受干扰素-γ和脂多糖诱导。到目前为止，还没有描述IP-10的功能。我们已经通过基因工程使肿瘤细胞分泌高水平的小鼠IP-10，并证明虽然IP-10在培养中对这些肿瘤细胞的生长没有影响，但它在体内引起了强大的宿主介导的抗肿瘤作用。IP-10的抗肿瘤反应是T淋巴细胞依赖的，非细胞自主的，并且似乎是通过由淋巴细胞、中性粒细胞和单核细胞组成的炎性浸润物的募集来介导的。这些结果证明了IP-10的一个重要的生物学特性，并提出了干扰素-γ和脂多糖的某些T细胞导向效应可能是由这种趋化因子介导的可能性。
IP-10 is a member of the -C-X-C-chemokine superfamily of proinflammatory cytokines whose secretion is induced by interferon gamma (IFN-gamma) and lipopolysaccharide (LPS). To date no function has been described for IP-10. We have genetically engineered tumor cells to secrete high levels of murine IP-10 and demonstrate that while IP-10 has no effect on the growth of these tumor cells in culture, it elicits a powerful host-mediated antitumor effect in vivo. The IP-10 antitumor response is T lymphocyte dependent, non-cell autonomous, and appears to be mediated by the recruitment of an inflammatory infiltrate composed of lymphocytes, neutrophils, and monocytes. These results document an important biologic property of IP-10 and raise the possibility that some of the T cell-directed effects of IFN-gamma and LPS may be mediated by this chemokine.