Th1／Th2细胞与自身免疫性疾病

Ｔｈ１／Ｔｈ２细胞与自身免疫性疾病刘俊铎综述刘志红审校关键词ＣＤ４＋细胞Ｔｈ１／Ｔｈ２细胞自身免疫性疾病中图法分类号Ｒ５９３．２人们根据ＣＤ４＋细胞产生的细胞因子的不同把它分为Ｔｈ１细胞和Ｔｈ２细胞。Ｔｈ１型细胞因子主要包括ＩＬ－２、ＴＮＦ－α、ＩＮ...     

血吸虫及其相关蛋白与自身免疫性疾病

自身免疫性疾病(ADs)是以特定的靶器官或多个器官系统的慢性损害和功能障碍为特征,临床上缺乏有效的治疗方法,目前发病率逐年升高,严重威胁人类健康。现有数据显示,血吸虫感染或注射血吸虫相关蛋白可能保护或减轻机体免受自身免疫性疾病的损害。研究学者已经建立相应的小鼠自身免疫疾病模型,证实了注射血吸虫蛋白具有诱导宿主Th2免疫偏移,下调Th17反应,并诱导旁路途经活化的巨噬细胞,从而减轻自身免疫性疾病,具有肯定的治疗效果。在这篇综述中,我们总结了血吸虫感染及血吸虫相关蛋白与减轻Th1介导的自身免疫性疾病之间的关系,力争明确其潜在的免疫保护机制。     

寄生虫感染对自身免疫性疾病的保护作用

流行病学调查表明在许多国家寄生虫感染率和自身免疫性疾病的发病率往往呈负相关,提示寄生虫感染对自身免疫性疾病可能有保护作用。早期的研究表明,Th1/Th2细胞活性的相对平衡对机体局部和全身的免疫及病理状况都有直接影响。自身免疫性疾病往往伴随着Th1细胞的过度活动;而蠕虫感染却常可诱导一个偏向于Th2细胞的反应。综合以上事实,有理由推测,某些寄生虫感染对某些自身免疫性疾病可能有一定的保护作用。     

Th17细胞与自身免疫性疾病

CD4 T细胞按照分化和功能特征分为辅助性T细胞1(Th1)、Th2和调节性T细胞(Treg)。Th1细胞主要分泌γ干扰素(IFN-γ)、IL-2和肿瘤坏死因子α(TNF-α)等细胞因子,介导细胞免疫,在抗细胞内感染的细菌、病毒和寄生虫等方面发挥重要作用;Th2型细胞通过分泌IL-4、IL-5、IL-10和IL-13等     

基因芯片与自身免疫性疾病

基因芯片技术是 90年代兴起的一项前沿生物技术 ,它将生物学中许多不连续的分析过程连续化 ,并使其微型化 ,具有无可比拟的高效、快速和多参量的特点 ,是传统的生物技术如检测、杂交、分型和ＤＮＡ测序的一次重大创新和突破。美国《科学》杂志把基因芯片评为 1998年世界十大科技突破之一。《财富》杂志给予基因芯片极高的评价 ,认为微处理机在本世纪使我们的经济结构发生了根本改变 ,给人类带来了巨大财富 ,改变了我们的生活方式。然而 ,基因芯片给人类带来的影响可能会更大 ,它可能从根本上改变医学行为和我们的生活质量 ,从而改变世界的面…     

自身免疫性疾病与发热

自身免疫性疾病是由于机体自身免疫反应导致的一大组疾病,其临床表现复杂多样,是导致发热的常见原因。 与感染、肿瘤性疾病一样,自身免疫性疾病是发热的重要鉴别诊断。不同自身免疫性疾病具有特征性临床表现,诊 断需要根据临床表现、自身抗体、影像及病理检查综合确立。治疗过程中应密切观察体温变化,及时调整治疗方案。     

抗原呈递细胞分泌的细胞因子与自身免疫性疾病

组织特异性自身免疫性疾病，包括多发性硬化症（MS）、类风湿性关节炎（RA）等，都是由于周围淋巴器官对自身抗原的耐受消失，导致自身反应性的效应细胞过度扩增，引起组织特异性炎症所致。虽然辅助性T细胞（Th）广泛参与了自身免疫性疾病的发生，但抗原呈递细胞（APC）才是自身免疫反应起始和恶化的最关键因素。APC在外周免疫中发挥多重作用，     

自身免疫性疾病

自身免疫性疾病（AID）是多种原因造成机体免疫功能紊乱,从而对自身抗原产生免疫应答,造成多系统损害的疾病。常规的糖皮质激素、免疫抑制剂及细胞毒性药物对危重或难治性AID疗效欠佳,近年来ASCT治疗危重或难治性自身免疫性疾病已在国内多中心进行。     

维生素D与自身免疫性疾病

随着肠、骨、肾等经典靶器官组织以外的一些组织的特异性维生素D受体的发现,维生素D的一些新功能亦逐渐为人们所认识。其中最引人注目的是维生素D的免疫调节功能。维生素D作用于免疫反应的多个环节,能够调节T细胞介导的多种免疫性疾病。1,25－（OH）2D3有可能作为一种新型的免疫调节剂达到防治自身免疫性疾病的作用,而不致引起广泛的免疫抑制。     

细胞因子检测与自身免疫性疾病

细胞因子 Cytokine,ck)是由免疫细胞和相关细胞产生的调节细胞功能的高活性多功能低分子量蛋白质 ,按结构可分为造血因子家族、干扰素家族、趋化因子家族、肿瘤坏死因子家族及其他因子家族 [1 ]。近年来对细胞因子参与自身免疫过程的机制 ,尤其是在 T细胞介导的自身免疫性疾病中的作用 ,已有了较为深入的研究 [2 ] 。1　细胞因子检测细胞因子的检测方法有三大类 ,即分子生物学测定法、生物活性测定法和免疫化学测定法。分子生物学测定法是测定细胞因子 m RNA的表达水平 ,采用多聚酶链反应 (PCR)。但此法需要特殊的实验设备 ,操作比较复…     

Mesenchymal stem cells and autoimmune diseases

Mesenchymal stem cell (MSC) immunosuppressive properties offer a potentially attractive therapeutic modality for autoimmune diseases. MSC inhibit virtually all types of immune responses in vitro and prevent the induction of disease in several experimental models of autoimmunity. However, the processes involved in the pathogenesis of human diseases are more complicated and treatment cannot be administered before disease induction. In autoimmune diseases persistent antigenic stimulation recruits endogenous MSC to the site of lesion that contribute to the fibrotic evolution. Therefore, administering MSC to a chronic inflammatory disorder may not be desirable. In fact, MSC are not constitutively immunosuppressive but require a 'licensing' step provided by molecules of acute phase inflammation, like IFNγ and TNF-α, or toll-like receptor (TLR) ligands. Conversely, different cytokines and/or the stimulation of selective TLR make MSC to become immunostimulatory. Therefore, dissecting the inflammatory environment in autoimmune diseases will identify the best conditions amenable to successful MSC therapy.     

Involvement of midkine in autoimmune and autoinflammatory diseases

Abstract

Midkine (MK) is a heparin-binding growth factor that markedly expressed during embryogenesis but downregulated to inconsiderable levels in healthy adults. However, MK is upregulated during tissue repair and in many pathologic conditions, mostly malignancies and inflammatory diseases. MK promotes a number of functions in target cells such as migration, proliferation, survival, growth, reproduction and repair, angiogenesis, and gene expression. It acts as a pro-inflammatory cytokine and contributes to chronic inflammation via promoting chemotaxis and tissue infiltration of neutrophils and macrophages. Furthermore, MK upregulated the production of various inflammatory mediators (i.e. interleukin (IL) 6 and IL8). Recent studies have demonstrated strong evidence that MK is involved in the onset and progression of autoimmune rheumatic diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and Sjögren’s syndrome (SS) and other autoimmune conditions such as multiple sclerosis (MS). Additionally, it has been shown that MK is overexpressed in two major clinically defined forms of inflammatory bowel diseases (IBD), Crohn’s disease (CD) and ulcerative colitis (UC), which are classified as autoinflammatory diseases. Taken together, MK is involved in the pathogenesis of autoimmune and autoinflammatory diseases and may serve as an indicator and biomarker in these conditions. Furthermore, MK inhibitors are expected to contribute in the management of these diseases.     

Haemopoietic stem cell transplantation in autoimmune diseases: a European perspective

The potential of haemopoietic stem cell transplantation (HSCT) for the treatment of autoimmune and inflammatory diseases was originally supported by almost three decades of animal experiments and by the serendipitous remissions of autoimmune disease observed in patients undergoing transplantation for haematological disorders. Improved safety of both autologous and allogeneic HSCT over the last decade has been followed by increasing acceptance of HSCT as an experimental treatment for severe autoimmune diseases that are resistant to conventional treatment. International databases have collated over 700 procedures performed specifically for a variety of autoimmune diseases. Phase III clinical trials are in progress for some diseases. This review provides a comprehensive update on the efficacy and toxicity of HSCT in severe autoimmune disease. Future directions in the context of other evolving therapies are discussed.     

Th1/Th2细胞平衡偏移与自身免疫性甲状腺疾病的相关性研究

目的 明确白细胞介素-2(IL-2)、IL-5与自身免疫性甲状腺疾病(AITD)发生的相关性,探讨Th1/Th2细胞平衡在自身免疫性甲状腺疾病发病中的作用.方法 选取2007年8月至2008年5月南昌大学第三附属医院内分泌科45例Graves病(GD)、30例桥本甲状腺炎(HT)患者,同时选取20名健康体检者作为对照组.采用酶联免疫吸附试验法(ELISA)检测患者和对照组血清中Th1型细胞因子IL-2扣Th2型细胞因子IL-5并进行统计学分析.结果 (1)GD患者血清中IL-5明显高于HT组和对照组(P<0.05),而IL-2与对照组相比差异无统计学意义(P>0.05).(2)HT患者血清IL-2明显高于GD组和对照组(P<0.05),而IL-5与对照组相比差异无统计学意义(P>0.05).(3)HT患者Th1型细胞因子IL-2与甲状腺球蛋白抗体(TCAb)和甲状腺微粒体抗体(TMAb)呈显著正相关(r=0.517,P<0.05;r=0.475,P<0.01).结论 Th1/Th2细胞免疫平衡在HT患者中以Th1细胞免疫占优势为主,在GD患者中以Th2细胞免疫占优势为主.     

自身免疫性肝病及其重叠综合征的诊断及治疗

自身免疫性肝病主要包括自身免疫性肝炎( autoimmune hepatitis,AIH)、原发性胆汁性肝硬化(primary biliary cirrhosis,PBC)、原发性硬化性胆管炎(primary sclerosing cholangitis,PSC)及其相互重叠的综合征,但就相互重叠关联而言尚没有明确的定义.在重叠综合征中,以AIH - PBC最为多见,在AIH或PBC患者中占10％[1].近年来由于相关临床经验的累积、实验室诊断技术的发展以及肝活检的普及,使得我国自身免疫性肝病检出率明显增高.     

Statins and autoimmune diseases

Inhibitors of 3‐hydroxy‐3methylglutaryl coenzyme A (HMG‐CoA) reductase or statins are effective lipid lowering drugs. The lipid lowering activity is mainly achieved through reduction of cholesterol synthesis and up‐regulation of low density lipoprotein receptors that in turn clear low density lipoproteins and low density lipoprotein precursors from the blood. HMG‐CoA reductase competitively blocks mevalonate, the enzyme reaction product that is the precursor not only of cholesterol but also of several non‐steroidal isoprenoid compounds. Isoprenoids allow the attachment to the cell membrane of signalling proteins involved in various cell functions; their inhibition explains the so‐called pleiotropic effects of statins, which include anti‐inflammatory, anticoagulant and immunomodulatory properties. Such pleiotropic activities have been suggested to justify the benefits of statin therapy besides the simple reduction in plasma cholesterol levels. Accelerated atherosclerosis has been reported in several autoimmune rheumatic diseases. Non‐traditional risk factors for atherosclerosis, such as inflammation, immune‐mediated responses and thrombophilia, have been suggested to play a major role in sustaining premature atherosclerosis in autoimmune rheumatic diseases. This review focuses on the potential use of statins as a new therapeutical tool for treating autoimmune rheumatic diseases based on their antiatherosclerotic activity and on their pleiotropic effect on inflammation, haemostasis and the immune responses.