T淋巴细胞与炎症性肠病

炎症性肠病与自身免疫密切相关, T淋巴细胞在其发病机制中承担了重要的角色。CD4 T细胞既可作为导致肠黏膜炎症的效应细胞、也可作为抑制肠黏膜炎症的调节细胞发挥作用。CD4 T细胞在IL-12的作用下极化为Th1, 形成IFN-γ、TNF-α升高的Th1型炎症; 在IL 13的作用下极化为Th2, 出现IL-4、IL-5升高的Th2型炎症。某些CD4 T分化为以分泌IL-10、TGF-β为主的调节细胞, 抑制肠黏膜炎症。CD8 T细胞在炎症性肠病中的作用目前尚不十分明确。此外, 肠黏膜上皮中某些特有的T细胞如CD4 CD8 αα双阳性细胞和γδT细胞也参与了肠黏膜炎症的调节。对T细胞的深入研究, 为炎症性肠病的治疗提供了免疫学方向和策略。     

肠道内Th17细胞的特征及其在炎症性肠病中的作用

Th17细胞是近几年发现的一类能够分泌白介素17(interleukin 17,IL-17)的CD4+T细胞,与自身免疫性疾病以及慢性炎症关系密切。Th17细胞在肠道内的增殖、分化、成熟具有一定的特征性,是肠道免疫屏障的重要组成部分,同时Th17细胞又能根据肠道内的变化分泌细胞因子来维持肠道免疫稳态,如IL-17、IL-22等。另一方面,肠道免疫机制异常在炎症性肠病的发病机制中占重要地位,Th17细胞及其相关细胞因子参与炎症性肠病的免疫反应,调节Th17细胞在肠道内的动态平衡对于治疗肠道疾病意义重大。本文就Th17细胞在肠道内的增殖分化、生物学功能、与炎症性肠病的关系以及关于Th17细胞动态平衡的调节做一综述。     

细胞因子在炎症性肠病免疫发病机理中的作用及在治疗中的应用前景

炎症性肠病发病机制复杂 ,细胞因子在炎症性肠病肠道炎症反应和粘膜免疫反应中起重要作用 ,本文就细胞因子在炎症性肠病免疫发病机制中的作用及在治疗中的应用前景作一综述。     

016 细胞因子在炎症性肠病免疫发病机理中的作用及在治疗中的应用前景

炎症性肠病发病机制复杂,细胞因子在炎症性肠病肠道炎症反应和粘膜免疫反应中起重要作用,本文就细胞因子在炎症性肠病免疫发病机制中的作用及在治疗中的应用前景作一综述.     

细胞因子在炎症性肠病免疫发病中的作用及在治疗中的应用前景

炎症性肠病发病机制复杂，细胞因子在炎症性肠病为症反应和粘膜免疫反应中起重要作用，本文就细胞因子在炎症性肠病免疫发病机制中的作用及在治疗中的应用前景作一综述。     

Th17细胞因子在炎性肠病发病机制中的研究进展

炎性肠病(IBD)的发病率越来越高,但其发病机制尚未完全明确,免疫机制异常在其发病机制中占有重要地位。既往人们认为Th1细胞和Th2细胞分泌的细胞因子失衡是造成IBD发病的主要原因,但是近年来发现了一种新的CD4+辅助T细胞亚群Th17,使IBD的发病机制得到了更好的解释。越来越多的研究表明,与Th17相关的一些细胞因子参与了炎性肠病的免疫反应。通过这些细胞因子在炎性肠病中的作用,更进一步揭示了炎性肠病的发病机制,为治疗炎性肠病提供新的思路。     

Th17细胞在炎症性肠病发病中作用的研究进展

炎症性肠病(inflammatory bowel diseases, IBD)的病因和发病机制尚不完全清楚, 免疫调节功能障碍在IBD的发病中起关键作用。辅助性T细胞(helper T cell, Th)是免疫系统的重要组成部分。当Th细胞分化不受调控及其细胞因子过度激活时, 免疫系统会转变成促炎状态, 进而诱发自身免疫性炎症。近年来, 越来越多的证据表明Th17细胞及其相关的细胞因子参与了IBD的发病。这些发现使Th17细胞及调节其发育和功能的途径成为治疗的靶点。文章就Th17细胞在IBD发病中的作用以及相关的治疗策略作一综述。     

IL-23/IL-17炎症轴与炎症性肠病的关系研究进展

肠黏膜慢性炎症损伤是炎症性肠病(IBD)的重要病变特点,研究表明白细胞介素23(IL-23)/IL-17炎症轴参与肠黏膜炎性损伤并参与IBD的发生、发展、治疗与转归.IL-23为IL-17重要上游分子,可促进Th17细胞活化、增殖和炎性细胞因子的分泌,并参与IBD病变局部中性粒细胞、单核巨噬细胞、调节性T细胞(Treg...     

肥大细胞与炎症性肠病

肥大细胞(MC)广泛分布于胃肠道,对胃肠粘膜分泌、吸收、粘膜血流、神经及平滑肌功能具有重要的调控作用.粘膜内MC数量及功能的改变、粘膜内IgE的作用、MC释放生物活性介质以及与神经、胃肠激素的相互作用等机制在炎症性肠病(IBD)的发生发展中有重要作用.MC稳定剂Ketotifen已应用于临床.     

肥大细胞与炎症性肠病

炎症性肠病（Inflammatoryboweldisease,IBD）包括溃疡性结肠炎（Ulcerativecolitis）和克罗恩病（Crohn’sdisease）,是一种原因不明的慢性非特异性肠道炎症,其发病机制主要和免疫、遗传、感染、应激等多种因素有关。近年来发现其发病与肥大细胞也密切相关。     

Th1, Th2, and Th17 cytokines in systemic lupus erythematosus

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the breakdown of immune tolerance leading to excessive inflammation and tissue damage. Imbalance in the levels of cytokines represents one of the multifactorial causes of SLE pathogenesis and it contributes to disease severity. Deregulated levels of T helper type 1 (Th1), type 2 (Th2), and type 17 (Th17) cytokines have been associated with autoimmune inflammation. Growing evidence has shown deregulated levels of Th1, Th2, and Th17 cytokines in SLE patients compared to healthy controls associated with disease activity and severity. In this review, we describe and discuss the levels of Th1, Th2, and Th17 cytokines in SLE patients, and clinical trials involving Th1, Th2, and Th17 cytokines in SLE patients. In particular, with the exception of IL-2, IL-4, and TGF-β1, the levels of Th1, Th2, and Th17 cytokines are increased in SLE patients associated with disease severity. Current phase II or III studies involve therapeutic antibodies targeting IFN-α and type I IFN receptor, while low-dose IL-2 therapy is assessed in phase II clinical trials.     

Th17 cells: interactions with predisposing factors in the immunopathogenesis of inflammatory bowel disease

Inflammatory bowel disease (IBD) is a chronic inflammatory state of the GI tract of unknown etiology. Classically, tissue injury in IBD is thought to be primarily mediated by Th1 cells in Crohn’s disease or Th2 cells in ulcerative colitis. The discoveries of new subsets of T-helper cells, especially Th17 cells, have revolutionized our understanding of the disease immunopathology. Th17 cells seem to affect both innate and adaptive immune responses by the release of regulatory cytokines. Understanding the role of Th17 cells in IBD pathogenesis and targeting their regulatory cytokines may provide potential therapeutic approaches for the treatment of IBD in the future.     

Increased intracellular Th1 cytokines in scid mice with inflammatory bowel disease

Severe combined immunodeficient (scid) mice engrafted with small pieces of full thickness gut wall from immunocompetent syngenic donors develop a chronic and lethal colitis. Lymphocytes from the lamina propria of engrafted mice were analyzed for phorbol ester/ionomycin-induced cytokine production by intracellular staining. A 4 – 5-fold increase in the fraction of IFN-γ-producing CD4+ lamina propria T cells was found in moderately and severely diseased mice when compared to healthy congenic C.B-17 control mice. The number of IL-2-producing T cells was increased by approximately 2-fold when comparing mice suffering from severe disease to healthy control mice. The fraction of TNF-α positive CD4+ T cells was increased by a factor of two in both moderately and severely diseased mice. When analyzing Th2 cytokines, it was found that the levels of IL-4-producing CD4+ T cells was not altered in diseased animals, whereas the fraction IL-10-producing CD4+ T cells was reduced by a factor of 20. The combined data showed a 15 – 25-fold increase in the Th1/Th2 ratio of diseased mice when compared to healthy control mice. No intracellular cytokines could be detected in lymphocytes not treated with phorbol ester/ionomycin. The present data identify a prominent role for Th1-type T helper cells in the immunopathogenesis of gut wall graft-induced inflammatory bowel disease in scid mice.     

细胞因子在炎症性肠病中作用机制的研究进展

炎症性肠病(IBD),包括克罗恩病和溃疡性结肠炎两种类型.它是在多种致病因素共同作用下由肠道免疫调节紊乱引发的炎症性疾病.近年来的研究发现,多种免疫细胞和细胞因子参与了两型IBD的发生和发展,其中ICE、辅助T细胞Th1/Th2在两型IBD中的功能和角色受到重视.对细胞因子在炎症性肠病中作用机制的深入研究为IBD的治疗提供了新的线索.     

Th17细胞与Treg细胞比例失衡在慢性炎症性疾病中研究进展

慢性炎症性疾病涉及许多疾病的发展过程,如变应性鼻炎、支气管哮喘、类风湿性关节炎（rheumatoid arthritis,R A）、炎症性肠病（inflammator y bowel disease,IBD）等。研究发现,Th17和Treg细胞通过其自身及产生的相应细胞因子,在慢性炎症性疾病发生发展过程中起着重要作用,而Th17和调节性T细胞（T Regulator Cell,Treg细胞）的分化共用了TGF-β这个细胞因子,提示他们在分化过程中有某种关联。本文旨在阐述Th17细胞与Treg细胞比例失衡在相关慢性炎症性疾病的发生发展中所起的关键作用。     

Th17 cytokines and mucosal immunity

Summary: The T-helper 17 (Th17) lineage is a recently described subset of memory T cells that is characterized by its CD4⁺ status and its ability to make a constellation of cytokines including interleukin-17A (IL-17A), IL-17F, IL-22, and, in humans, IL-26. Although most extensively described in the autoimmunity literature, there is growing evidence that the Th17 lineage plays a significant role in mediating host mucosal immunity to a number of pulmonary pathogens. This review highlights our current understanding of the role of the Th17 lineage and Th17 cytokines in mediating mucosal immunity to both pulmonary and gastrointestinal pathogens. While we have the strongest evidence that the Th17 lineage is centrally involved in mediating the host response to Gram-negative extracellular pulmonary pathogens, this literature is rapidly evolving and demonstrates a central role for Th17 cytokines both in primary infection and in recall responses seen in vaccine studies. In this review, we summarize the current state of this literature and present possible applications of Th17-targeted immunotherapy in the treatment and prevention of infection.     

Histologic mimics of inflammatory bowel disease

This review summarizes a variety of clinical and histologic mimics of idiopathic inflammatory bowel disease. All the entities that are included demonstrate one or more histologic features typical of idiopathic inflammatory bowel disease that may lead to potential diagnostic confusion and misinterpretation by the pathologist. The elements of the clinical history, laboratory test results, and endoscopic findings that are helpful to the surgical pathologist in considering a diagnosis other than idiopathic inflammatory bowel disease are emphasized. On occasion, a poor response to standard treatment for idiopathic inflammatory bowel disease is the clue that prompts reconsideration of the initial diagnosis. Subtle histologic features, special stains, or other diagnostic methodologies that can aid in proper diagnosis are also discussed.     

同型半胱氨酸与炎症性肠病相关性血栓疾病的研究现状

目的 探讨同型半胱氨酸(Hcy)对炎症性肠病(IBD)患者的影响,为IBD相关性血栓疾病的深入研究提供参考.方法 在PubMeb、Medline、EMbase、CNKI、CBM数据库中检索1993年1月-2013年12月关于Hcy与IBD相关性血栓疾病的研究成果,进行分析总结.结果 IBD患者因反复炎症活动及高凝状态,增加了血栓形成的风险.高同型半胱氨酸血症(HHcy)在IBD相关性血栓疾病损伤机制中,主要通过氧化损伤血管内皮和体内抗凝系统失衡参与IBD相关性血栓形成的病理生理过程.HHcy是血栓形成的独立危险因素之一.结论 IBD患者血栓形成是一个复杂的病理过程,受多因素影响.Hcy在IBD相关性血栓疾病损伤机制中具有重要作用,其确切机制有待进一步研究.