炎症性肠病免疫学发病机制研究进展

<正>炎症性肠病是存在于胃肠道的炎症,以慢性复发性免疫系统激活为特点.炎症性肠病包括2种类型,即溃疡性结肠炎和克罗恩病[1],它是世界范围内影响人类健康的问题之一,常见于欧美地区,我国尚无普通人群的流行病学资料.Zhao等[2]的研究结果表明,炎症性肠病在中国也有很高的发生率.早在1623年和1852年克罗恩病和溃疡性结肠炎就被分     

炎症性肠病的免疫调控研究进展

炎症性肠病(IBD)是一类高发、病因尚未明确的慢性自身免疫性疾病,在全世界范围内发病率呈上升趋势。肠道微环境稳态失衡、免疫功能失调、环境变化或遗传因素都可能导致疾病的发生。免疫细胞,如巨噬细胞、树突状细胞、固有淋巴细胞以及T细胞、B细胞在IBD中发挥重要作用。巨噬细胞或树突状细胞通过上调炎症细胞因子表达,T细胞、B细胞通过分泌细胞因子或抗体参与IBD免疫调控。阐明IBD免疫作用的机制,可能为IBD的治疗提供新靶点。     

调节性T细胞在炎症性肠病中的研究进展

调节性T细胞(Treg)是一类具有免疫调节功能的T细胞亚群,可通过直接接触和细胞因子依赖等方式下调机体免疫反应,维持自身免疫耐受。近年来,Treg细胞在炎症性肠病中的作用越来越受到关注,本文总结并讨论了CD4 CD25 Treg细胞在炎症性肠病免疫方面的研究进展。     

炎症性肠病免疫学研究新知Ⅱ

炎症性肠病（Inflammatory Bowel Diseases,IBD）包括溃疡性结肠炎（ulcerative colitis,UC）和克罗恩病（Crohn’disease,CD）,是以肠道炎症为特征的免疫应答失调相关性疾病。免疫学病因方面作为IBD发病机制的重要组成部分,成为全球研究的热点。继上一篇报道后我们现就2010～2011上半年最新文献作简要介绍。     

滤泡辅助性T细胞与炎症性肠病相关的研究进展

炎症性肠病的病因及其发病机制尚未完全清楚,目前大多数研究表明是由多种因素相互作用引起,主要包括环境改变、遗传易感、细菌及病毒感染和自身免疫等各种因素,其发病机制主要表现为遗传易感人群在生物、心理、社会等环境因素的影响下,由肠道多种微生物启动肠道的先天免疫反应及后天获得性免疫反应,破坏肠黏膜免疫系统,引起消化道溃疡反复发作、炎性增生坏死等病理生理的改变,其中肠黏膜异常免疫反应引起的炎性改变在炎症性肠病的发病中起到重要作用.滤泡辅助性T细胞的异常表达与自身免疫性疾病密切相关,滤泡辅助性T细胞及其主要细胞因子在炎症性肠病起病及进展的免疫调节过程中发挥了关键作用.     

炎症性肠病动物模型的研究进展

炎症性肠病(IBD)包括溃疡性结肠炎和克罗恩病,发病较多,临床迄今尚无彻底治愈方法,患病率国内外均呈上升趋势。动物模型对研究IBD机制,筛选药物有重要意义。本文结合IBD发病的微生态学改变和免疫紊乱特征,对国内IBD造模方法进行综述,为最终建立符合人类IBD发病机理和临床表现的新型动物模型打基础。     

调节性T细胞在炎症性肠病中研究新进展

调节性T细胞是一类具有免疫调节并维持免疫稳定的T细胞亚群,可以通过直接触和细胞因子依赖等方式下调机体免疫反应。炎症性肠病是一类病因未明,侵及胃肠道的自身免疫性疾病,发病率在我国近年来有上升趋势,对炎症性肠病发病机制的研究成为热点,其中调节性T细胞扮演的角色备受关注,本文总结并讨论了调节性T细胞在炎症性肠病发病机制中的研究进展,为炎症性肠病免疫治疗寻求更多依据。     

调节性T细胞在炎症性肠病中研究新进展

调节性T细胞是一类具有免疫调节并维持免疫稳定的T细胞亚群,可以通过直接触和细胞因子依赖等方式下调机体免疫反应。炎症性肠病是一类病因未明,侵及胃肠道的自身免疫性疾病,发病率在我国近年来有上升趋势,对炎症性肠病发病机制的研究成为热点,其中调节性T细胞扮演的角色备受关注,本文总结并讨论了调节性T细胞在炎症性肠病发病机制中的研究进展,为炎症性肠病免疫治疗寻求更多依据。     

炎症性肠病与肠粘膜免疫

炎症性肠病（inflammatory bowel disease,IBD）包括溃疡性结肠炎（ulcerative colitis,UC）和克罗恩病（Crohn’s disease,CD）,是一组反复发作的非特异性的慢性肠道炎症性疾病,其病因尚未完全阐明。近年来,肠道共生菌与肠上皮屏障之间的关系及其驱动的肠粘膜免疫失衡的研究已取得很大的进展,对揭示IBD的病因和发病机制无疑有所裨益。     

树突状细胞在炎症性肠病中的作用研究进展

<正>炎症性肠病(IBD)是以慢性、复发性肠道炎症为特征的疾病,包括克罗恩病和溃疡性结肠炎,它的发病原因及机制尚不明确[1].树突状细胞 (DCs)是迄今为止发现的抗原提呈能力最强的一类专职的抗原提呈细胞 (APC),它在启动免疫应答与诱导耐受过程中发挥关键作用[2-3].肠道DCs在识别细菌、诱导耐受及T细胞分化中起重要作用.本文就DCs在IBD中的作用研究进展进行了综述,旨在为临床预防与治疗IBD提供依据.     

基于基因敲除的炎性肠疾病复合动物模型研究进展

建立合适的动物模型对于研究炎症性肠疾病（IBD）的机制以及探索新的治疗途径具有重要意义。单敲除某些与人类IBD易感性相关的基因并不表现为IBD的症状或症状较轻,而结合其他造模因素建立的复合动物模型能更好地模拟IBD的临床特征。本文主要介绍了三类新型复合动物模型的具体特点：基因双重敲除动物模型较单基因敲除模型的建立周期更短、疾病症状更明显;螺杆菌复合基因敲除模型有助于研究微生物感染在IBD发病机制中的作用;在基因敲除的基础上特异性缺失某种免疫细胞可用于研究该免疫细胞在IBD发展中的作用。这些模型在一定程度上有助于探索IBD的机制,其中Muc2/IL-10双重敲除模型有望成为IBD遗传学研究的重要动物模型。     

血小板活化与炎症性肠病

血小板的种系发生提示其在免疫炎症中起重要作用,近年来发现血小板活化与炎症性肠病的活动性密切 相关,活化的血小板可以释放炎症介质,表达介导炎症反应的表面分子,可与白细胞和内皮细胞发生相互作用,这 为抗血小板药物治疗炎症性肠病提供了理论依据。     

Chronic inflammatory bowel disease in childhood

The diagnosis of Crohn's disease in childhood has been facilitated by the use of fibreoptic endoscopy with biopsies, complemented by double-contrast radiology. Clinical suspicion leads initially to several relevant blood tests. These are followed by endoscopy and multiple colonic biopsies or barium follow-through studies depending on whether large-bowel or small-bowel disease is suspected. The present approach to diagnosis is based on corroborative investigative techniques-endoscopy, radiology, and histology, The availability of paediatric colonoscopes of small diameter should make it possible for paediatricians to perform limited examinations, but when more extensive endoscopy is indicated the child should be referred to special centres.     

Mucins and inflammatory bowel disease

There is a layer of mucus lining the gastrointestinal tract, which acts as both a lubricant and as a physical barrier between luminal contents and the mucosal surface. The mucins that make up this layer consist of a protein backbone with oligosaccharides attached to specific areas of the protein core. These areas are called the variable number tandem repeat regions. The degree of glycosylation of the mucins is central to their role in the mucus barrier. The oligosaccharides are variable and complex. It has been demonstrated that the degree of sulphation and sialylation and the length of the oligosaccharide chains all vary in inflammatory bowel disease. These changes can alter the function of the mucins. Mucins are broadly divided into two groups, those that are secreted and those that are membrane bound. The major mucins present in the colorectum are MUC1, MUC2, MUC3, and MUC4. Trefoils are a group of small peptides that have an important role in the mucus layer. Three trefoils have been demonstrated so far. They seem to play a part in mucosal protection and in mucosal repair. They may help to stabilise the mucus layer by cross linking with mucins to aid formation of stable gels. Trefoils can be expressed in the ulcer associated cell lineage, a glandular structure that can occur in the inflamed mucosa. There seem to be differences in the expression of trefoils in the colon and the small bowel, which may imply different method of mucosal repair.     

Management of inflammatory bowel disease

Ulcerative colitis and Crohn's disease result from an interaction between genetic and environmental factors. Only one gene, NOD2/CARD15, has been clearly identified; a minority of people with alteration of this gene develop Crohn's disease. The NOD2/CARD15 protein is thought to be involved in defence against intracellular bacteria. This supports the idea that Crohn's disease and ulcerative colitis result from altered immunological responses to the normal intestinal flora. Life expectancy is normal in ulcerative colitis and nearly so in Crohn's disease, but both conditions cause considerable morbidity. Approximately 80% of patients with Crohn's disease eventually require surgery, and about 25% of patients with ulcerative colitis require colectomy. Treatment of ulcerative colitis is generally by corticosteroids for acute disease and mesalazine for maintenance, but the range of therapies for Crohn's disease is expanding. Alternative therapies include immunosuppressives, enteral nutrition, antibiotics, anti-TNF antibody (infliximab), corticosteroids, and surgery. High dosages of corticosteroids may provide symptomatic relief in Crohn's disease but do not affect the long term natural history of the disease, and management strategies should avoid using steroids whenever possible.     

Cytomegalovirus and inflammatory bowel disease

An 80 year old man was admitted to hospital with a 4 month history of diarrhoea with blood and mucus. The diarrhoea could not be controlled by a variety of drugs and he died 7 weeks later. Rectal biopsy showed both intranuclear and intracytoplasmic inclusional bodies consistent with cytomegalovirus infection.