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IP-10,一种CXC趋化因子,在体内引发强大的胸腺依赖性抗肿瘤反应。

IP-10, a -C-X-C- chemokine, elicits a potent thymus-dependent antitumor response in vivo.

作者信息

Luster A D, Leder P

机构信息

Department of Genetics, Harvard Medical School, Boston, Massachusetts.

出版信息

J Exp Med. 1993 Sep 1;178(3):1057-65. doi: 10.1084/jem.178.3.1057.

Abstract

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.

摘要

IP-10是促炎细胞因子-C-X-C-趋化因子超家族的成员,其分泌由干扰素γ(IFN-γ)和脂多糖(LPS)诱导。迄今为止,尚未描述IP-10的功能。我们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对这些肿瘤细胞在培养中的生长没有影响,但它在体内引发了强大的宿主介导的抗肿瘤作用。IP-10的抗肿瘤反应依赖于T淋巴细胞,是非细胞自主性的,并且似乎是由由淋巴细胞、中性粒细胞和单核细胞组成的炎性浸润的募集介导的。这些结果证明了IP-10的重要生物学特性,并增加了IFN-γ和LPS的一些T细胞导向作用可能由这种趋化因子介导的可能性。

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