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| 1 | Genetic update on inflammatory factors in ulcerative colitis: Review of the current literature显示文摘Ulcerative colitis(UC) is one of the main types of inflammatory bowel disease, which is caused by dysregulated immune responses in genetically predisposed individuals. Several genetic factors, including interleukin and interleukin receptor gene polymorphisms and other inflammation-related genes play central role in mediating and modulating the inflammation in the human body, thereby these can be the main cause of development of the disease. It is clear these data are very important for understanding the base of the disease, especially in terms of clinical utility and validity, but summarized literature is exiguous for challenge health specialist that can used in the clinical practice nowadays. This review summarizes the current literature on inflammationrelated genetic polymorphisms which are associated with UC. We performed an electronic search of Pubmed Database among publications of the last 10 years, using the following medical subject heading terms: UC, ulcerative colitis, inflammation, genes, polymorphisms, and susceptibility. | Patricia Sarlos Erzsebet Kovesdi Lili Magyari Zsolt Banfai Andras Szabo Andras Javorhazy Bela Melegh | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 15 |
| 2 | NF-κB信号通路与炎症性肠病显示文摘炎症是多种细胞及细胞因子参与的机体防御性反应,但严重或长期的炎症则会造成机体损伤.炎症性肠病(inflammatory bowel disease,IBD)是一组以慢性、周期性炎症为特征的胃肠道疾病,长期、反复的胃肠道炎症不仅影响患者生活质量,而且增加了肠道纤维化及癌变的风险,而核因子Kappa B(nuclear factor-kappa B,NF-κB)与炎症反应关系非常密切.本文就NF-κB信号通路与IBD的联系作一简要概述. | 张善金 李弼民 | 2011 | 世界华人消化杂志2011，19，5： | 10 |
| 3 | Immunogenetic biomarkers in inflammatory bowel diseases:Role of the IBD3 region显示文摘Many studies have demonstrated the linkage between the IBD3 region(6p21.1-23),an area which encompasses the famous human leukocyte antigen(HLA) complex,and Crohn's disease(CD) or ulcerative colitis(UC).IBD3 is the only region that meets genome-wide significance,and provides stronger evidence of the linkage than 16p13.1-16q12.2(IBD1),the locus that contains the susceptibility gene CARD15.However,despite these findings,IBD3 susceptibility genes remain elusive and unclear due to the strong linkage disequilibrium,extensive polymorphism,and high gene density that characterize this area and also due to varying allele frequencies in populations around the world.This area presents an extremely high abundance of genes,including the classical and non-classical major histocompatibility complex(MHC) class Ⅰ and Ⅱ genes,and other genes,namely MHC class Ⅲ genes tumor necrosis factor(TNF)-α and-β,and Hsp,whose proteins play key functions in immunological processes.To date,it is not clear which genes within the MHC family contribute to the IBD pathogenesis,although certain HLA alleles have been associated with IBD.Recent insights into the biological function of other genes encoded within the IBD3 region,such as the MHC class Ⅰ chain-related(MIC) genes,have led investigators to a more comprehensive exploration of this region.MHC class Ⅰ chain-related molecule A(MICA) is highly polymorphic and interacts with NKG2 D,its receptor on the surface of NK,Tγδ and T CD8+ cells.Increased expression of MICA in intestinal epithelial cells and increased expression of NKG2 D in CD4+ T cells(lamina propria) in patients with CD have also been reported.MICA alleles have also been associated with IBD,and a variation at amino acid position 129 of the α2-heavy chain domain seems to categorize MICA alleles into strong and weak binders of NKG2 D receptor,thereby influencing the effector cells' function.In this regard,a relevant role of MICA-129-Val/Met single nucleotide polymorphism has recently been implicated in the pathogenesis of IBD.TNF-α and-β also play an important role in inflammatory response.In fact,IBD is commonly treated with TNF-α inhibitors.Additionally,polymorphisms of TNF-α gene are known to affect the gene expression level and particular TNF-α genotypes may influence the response of IBD patients treated with TNF-α inhibitors. | Manuel Muro Ruth López-Hernández Anna Mrowiec | 2014 | World Journal of Gastroenterology2014，20，41： | 6 |
| 4 | 脂多糖诱导的肿瘤坏死因子(LITAF)生物学功能研究进展显示文摘脂多糖诱导的肿瘤坏死因子(LPS-induced TNF-α,LITAF),又称p53诱导基因7或溶酶体/晚期内体小膜内在蛋白。早期研究认为,p53蛋白的164~170位氨基酸肽段导入到人体单核细胞后可抑制LITAF的表达。近期研究发现,LITAF在LPS诱导的单核细胞或巨噬细胞中作为炎症细胞因子TNF-α的转录激活剂起作用,进而引发炎症。典型的LITAF结构域包含N-端的CXXC区、25个氨基酸长的疏水区和C-端的(H)XCXXC区。当机体受到LPS刺激后,LITAF疏水区结合到胞膜上,将N-端和C-端的CXXC区域连接在一起,形成紧密结合的Zn2+结构,此结构域诱导LITAF蛋白和STAT6(B)蛋白形成复合体进入细胞核,与TNF-α的启动子结合进而激活细胞因子TNF-α的转录表达,内源性增强机体清除肿瘤细胞或入侵病原的能力。该文就LITAF的结构和生物学功能的研究进展进行概述。 | 张秀梅 李成华 | 2015 | 中国细胞生物学学报2015，37，4： | 3 |
| 5 | 炎症性肠病的研究现状显示文摘炎症性肠病(IBD)首先在北欧和北美洲人群中发现,以后在世界各地均有报道[1]。IBD是一类病因尚未明确的慢性非特异度肠道炎症,包括溃疡性结肠炎(UC)和克罗恩病(CD),临床表现为反复腹痛、腹泻、黏液血便。近年来我国的IBD发病率不断增高[2],可能是环境、遗传、感染、免疫、内脏的敏感性及精神因素等多因素相互作用所致[3]。随着治疗方案的不断改进及生物制剂的应用。 | 张兰兰 牛润章 司依馨 | 2012 | 中国实用内科杂志2012，32，S2： | 3 |
| 6 | TNF-TNF-α-308G/A-308G/A多态性与炎症性肠病易感性的Meta分析显示文摘目的系统评价肿瘤坏死因子-α(TNF-α)-308G/A多态性与炎症性肠病发病风险的相关性。方法计算机检索Pub Med、EMbase、CNKI、Wan Fang Data、CBM和VIP数据库,查找关于TNF-α-308G/A多态性与炎症性肠病易感性的病例-对照研究,检索时限均从建库至2015年1月25日。由2位评价员按照纳入与排除标准独立筛选文献、提取资料并评价纳入研究的方法学质量后,采用Rev Man 5.2和Stata 12.0软件进行Meta分析。结果最终纳入20个研究,共计2 860例患者和5 033例对照。Meta分析结果显示:与基因型GG比较,基因型GA、AA、GA+AA会增加溃疡性结肠炎的发病风险[GA vs.GG:OR=1.45,95%CI(1.02,2.07),P=0.04;AA vs.GG:OR=2.01,95%CI(1.32,3.05),P=0.001;GA+AA vs.GG:OR=1.51,95%CI(1.07,2.13),P=0.02];与基因型GA+GG比较,基因型AA会增加溃疡性结肠炎的发病风险[AA vs.GA+GG:OR=1.92,95%CI(1.26,2.91),P=0.002];等位基因A与溃疡性结肠炎发病风险无关。与基因型GG比较,基因型AA会增加克罗恩病的发病风险[AA vs.GG:OR=1.49,95%CI(1.07,2.08),P=0.02];与基因型GA+GG比较,基因型AA会增加克罗恩病的发病风险[AA vs.GA+GG:OR=1.50,95%CI(1.08,2.09),P=0.02]。基因型GA、GA+AA及等位基因A与克罗恩病发病风险无关。按人种来源的亚组分析显示,欧洲人TNF-α-308G/A基因多态性与炎症性肠病相关。结论现有证据表明,TNF-α-308G/A基因多态性与炎症性肠病易感性相关,基因型GA、AA、GA+AA均会增加溃疡性结肠炎的发病风险;基因型AA会增加克罗恩病的发病风险。鉴于纳入研究数量有限,上述结论尚需开展更多研究予以验证。 | 柳舟 董卫国 王军 张吉翔 郭绪峰 | 2015 | 中国循证医学杂志2015，15，4： | 3 |
| 7 | Genetic polymorphisms predict response to anti-tumor necrosis factor treatment in Crohn's disease显示文摘AIM To investigate genetic factors that might help define which Crohn's disease(CD) patients are likely to benefit from anti-tumor necrosis factor(TNF) therapy. METHODS This was a prospective cohort study. Patients wererecruited from a university digestive disease practice database. We included CD patients who received antiTNF therapy,had available medical records(with information on treatment duration and efficacy) and who consented to participation. Patients with allergic reactions were excluded. Patients were grouped as ever-responders or non-responders. Genomic DNA was extracted from peripheral blood,and 7 single nucleotide polymorphisms(SNPs) were assessed. The main outcome measure(following exposure to the drug) was response to therapy. The patient genotypes were assessed as the predictors of outcome. Possible confounders and effect modifiers included age,gender,race,and socioeconomic status disease,as well as disease characteristics(such as Montreal criteria). RESULTS121 patients were included. Twenty-one were nonresponders,and 100 were ever-responders. Fas ligand SNP(rs763110) genotype frequencies,TNF gene-308 SNP(rs1800629) genotype frequencies,and their combination,were significantly different between groups on multivariable analysis controlling for Montreal disease behavior and perianal disease. The odds of a patient with a Fas ligand CC genotype being a non-responder were four-fold higher as compared to a TC or TT genotype(P = 0.009,OR = 4.30,95%CI: 1.45-12.80). The presence of the A(minor) TNF gene-308 allele correlated with three-fold higher odds of being a non-responder(P = 0.049,OR = 2.88,95%CI: 1.01-8.22). Patients with the combination of the Fas ligand CC genotype and the TNF-308 A allele had nearly five-fold higher odds of being a non-responder(P = 0.015,OR = 4.76,95%CI: 1.35-16.77). No difference was seen for the remaining SNPs.CONCLUSION The Fas-ligand SNP and TNF gene-308 SNP are associated with anti-TNF treatment response in CD and may help select patients likely to benefit from therapy. | Uri Netz Jane Victoria Carter Maurice Robert Eichenberger Gerald Wayne Dryden Jianmin Pan Shesh Nath Rai Susan Galandiuk | 2017 | World Journal of Gastroenterology2017，23，27： | 1 |
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