Limongi F
Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Clin Ter. 2015;166(2):e122-5. doi: 10.7417/CT.2015.1834.
T- helper 1 (Th1) cytokines and chemokines in primary biliary cirrhosis (PBC) has been investigated in several studies. The involvement of (C-X-C motif) receptor 3 (CXCR3) and its ligands in the pathogenesis of PBC was studied in autoimmune cholangitis animal models suggesting that CXCR3 chemokines contribute to the development of PBC. In humans with PBC, interferon (IFN)γ-induced protein 10 (IP-10) and chemokine (C-X-C motif) ligand 9 (MIG) expressions, and CXCR3-positive cells were present in the portal areas of diseased livers. MIG and IP-10 were positively associated with the severity of liver fibrosis. Circulating IP-10 and MIG levels, and CXCR3-expressing cells, in PBC were increased significantly compared to controls and appeared to increase with disease progression. Furthermore, a significant reduction of these chemokines in PBC patients' serum after ursodeoxycholic acid (UDCA) treatment has been shown.
多项研究对原发性胆汁性肝硬化（PBC）中的辅助性T细胞1（Th1）细胞因子和趋化因子进行了调查。在自身免疫性胆管炎动物模型中研究了（C-X-C基序）受体3（CXCR3）及其配体在PBC发病机制中的作用，提示CXCR3趋化因子促成了PBC的发展。在患有PBC的人类中，干扰素（IFN）γ诱导蛋白10（IP-10）和趋化因子（C-X-C基序）配体9（MIG）的表达以及CXCR3阳性细胞存在于病变肝脏的门管区。MIG和IP-10与肝纤维化的严重程度呈正相关。与对照组相比，PBC患者循环中的IP-10和MIG水平以及表达CXCR3的细胞显著增加，且似乎随疾病进展而升高。此外，已表明熊去氧胆酸（UDCA）治疗后PBC患者血清中这些趋化因子显著减少。
