γ-干扰素诱生蛋白10与肝病关系研究进展

摘要

Interferon (IFN)-γ-induced protein 10 (IP-10/CXCL10) and its receptor CXCR3,appear to contribute to the pathogenesis of viral hepatitis. CXCL10 could be secreted by various cells,including T cells,NK cells,endothelial cells, hepatocytes,etc. It plays an essential role in recruiting specific T cells,NK cells and other effector cells to local inflammatory sites to control the infection by through direct or indirect interactions. IP-10 expression is also correlated with developing liver fibrosis and cirrhosis from viral hepatitis. Furthermore,high level of IP-10 in baseline has shown a clinical utility as a predictor of effective outcome of anti-viral therapy. Since the mechanism of how IP-10 modulates anti-viral responses remains unknown, further studies are still needed to investigate the interaction between IP-10 and leukocytes in the pathogenesis of hepatitis,and to evaluate whether IP-10 could be a novel therapeutic target of viral diseases.%趋化因子γ-干扰素诱生蛋白10（IP-10)和它的受体CXCR3在肝炎的发生发展过程中起重要作用，并可能对抗病毒治疗疗效的判断提供有益的线索。IP-10可以由多种细胞分泌，如T淋巴细胞、NK细胞、内皮细胞和肝实质细胞等。在病毒性肝炎发生的过程中，IP-10通过直接或间接作用于病毒特异性T细胞和NK细胞等效应细胞，趋化它们到肝组织局部发生免疫应答，发挥抗病毒作用。IP-10的分泌同时也会促进病毒性肝炎发展成为肝纤维化、肝硬化。在抗病毒药物治疗的患者中，血清基线IP-10水平与治疗后病毒DNA载量以及抗原滴度呈负相关关系，对于抗病毒药物治疗后免疫应答反应起了一定的预测作用。IP-10在肝病的发生发展过程中的具体作用机制还需要更深入的研究。