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Primary biliary cholangitis （PBC） is a liver autoimmune disease with a strong genetic tendency characterized by the degeneration and necrosis of bile duct epithelial cells， and it is often observed in middle-aged and elderly women. With the continuous development of genome-wide association studies， the genetic susceptibility of PBC has attracted more and more attention. This article elaborates on the research advances in the genetic susceptibility genes closely associated with PBC， in order to provide effective targets for the treatment of PBC.
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Primary biliary cholangitis （PBC） is a chronic autoimmune disease of cholestasis in which immune factors lead to progressive small bile duct destruction， cholestasis， and eventually liver fibrosis， liver cirrhosis， and even liver failure. Macrophages， as a group with functional heterogeneity， play different roles in the whole disease process of PBC. This article summarizes the possible ways by which macrophages are involved in the pathogenesis of PBC and discusses their impact on the disease and the potential therapeutic targets of macrophages. It is pointed out that macrophages are mainly involved in innate immunity in PBC injury and are associated with gut microbiota dysbiosis， and they are also associated with cholestasis， liver fibrosis， and liver cirrhosis in the later stages of the disease.
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Primary biliary cholangitis (PBC) is a chronic cholestatic liver disease, and may progress to cirrhosis and associated with complications of end-stage liver disease. The immunological characteristic of PBC is the presence of anti-mitochondrial autoantibodies (AMAs), and some anti-nuclear antibodies (ANAs) have high specificity for the diagnosis of PBC. In recent years, it has been found that anti-gp210, anti-sp100 and anti-centromere antibodies are correlated with the severity of PBC, treatment response to ursodeoxycholic acid (UDCA) and poor prognosis. However, correlation between AMAs and disease progression of PBC is still in controversial. This article reviewed the progress in research on the influence of autoantibodies on biochemical response and prognosis of PBC.
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Objective To investigate the correlation between ADAM33 T1, S2 gene polymorphism and Bronchial asthma risk in china. Methods We retrived the relevant published studies about ADAM33 T1, S2 gene polymorphism and bronchial asthma risk. Then we divided the population into Chinese and other Asian population. Odds ratio (OR) of Case group and control group was selected as the effect index. Stata 11.0 software was used to calculate heterogeneity test, ORs and 95%CI of two areas, and gave the forest plot and funnel plot of meta results. Results A total of 27 studies were included in this analysis,18 studies in ADAM33 T1 site were 3881 cases in case group, and 3780 cases in control group;and 14 studies in ADAM33 S2 site were 3222 cases in case group, and 3513 cases in control group. Additive model, dominant model, recessive model of ADAM33 T1 in Chinese had association with the susceptibility of bronchial asthma. The results were OR=1.488, 95% CI:1.002-2.167 in Additive model, OR=1.619, 95%CI:1.059-2.475 in dominant model;OR=2.523, 95%CI:1.910-3.333 in recessive model. Three models of ADAM33 T1 in other Asian country had no association with the susceptibility of Bronchial Asthma. Three gene model of ADAM33 S2 in Asian had no association with bronchial asthma susceptibility. Except ADAM33 T1 polymorphism in recessive model, other mode of T1, S2 had no publication bias in Chinese population. Conclusion There are association between ADAM33 T1 gene polymorphism and bronchial asthma, but ADAM33 S2 gene polymorphism and bronchial asthma have no association in Chinese population.
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<p><b>OBJECTIVE</b>To investigate the effects of interleukin-17 (IL-17) on the proliferation, transformation and collagen synthesis of the lung fibroblasts in mice with bleomycin-induced pulmonary fibrosis.</p><p><b>METHODS</b>In a mouse model of pulmonary fibrosis established by intratracheal administration of 5 mg/kg bleomycin, the dynamic expressions of IL-17/IL-17 receptor (IL-17R) mRNAs were detected by RT-PCR. At 14 days following bleomycin administration, the pulmonary fibroblasts were isolated, cultured and identified. MTT assay was used to assess the proliferation of the pulmonary fibroblasts in response to IL-17 treatment at different concentrations, and RT-PCR and Western blotting were employed to examine the mRNA and protein expressions of α-smooth muscle actin (α-SMA) and types I and III collagen.</p><p><b>RESULTS</b>IL-17/IL-17R mRNA levels were increased obviously in the pulmonary fibroblasts of rats with pulmonary fibrosis, and the highest expressions occurred at 14 days following bleomycin administration. Exogenous IL-17, at the optimal concentration of 50 ng/ml, significantly promoted the proliferation of the pulmonary fibroblasts in primary culture and obviously increased α-SMA expression and types I and III collagen synthesis in the fibroblasts.</p><p><b>CONCLUSION</b>IL-17 can promote the proliferation, transformation, and collagen synthesis of the pulmonary fibroblasts from rats with bleomycin-induced pulmonary fibrosis.</p>