血吸虫与宿主相互关系的研究进展

血吸虫侵入宿主后对宿主产生损害,同时宿主会设法清除感染的血吸虫,血吸虫与宿主相互作用于对方,在长期共进化中形成了复杂的相互适应机制.近年来,血吸虫-宿主相互关系中研究较多的是免疫学关系,如宿主免疫调节、血吸虫免疫逃避等.血吸虫谷胱苷肽S转移酶等分子对宿主具有免疫保护性作用.     

血吸虫感染致Th1/Th2效应选择及其抗感染作用的分子机制

血吸虫感染导致宿主体内CD4 + T细胞的高度极化反应 ,产生优势的Th1或Th2功能亚群 ,分泌不同的细胞因子 ,分别介导细胞免疫和体液免疫 ,在宿主的抗感染保护性免疫中发挥重要作用 ,这对血吸虫疫苗的研制具有重要的指导意义。而血吸虫感染动物模型为Th1和Th2极化的免疫效应研究提供了特异而有效的研究工具。     

IL—12抗血吸虫作用的研究进展

血吸虫感染激发宿主产生免疫应答 ,其机制非常复杂。IL- 12作为一个多功能的免疫调节因子 ,通过调节 NK细胞、巨噬细胞的活性和 Th细胞、细胞毒性 T细胞介导的特异性免疫作用 ,在机体感染血吸虫早期的非特异性免疫和随后的抗原特异性免疫过程中起到了极重要的作用。一些研究表明 ,IL - 12对血吸虫虫卵肉芽肿形成及肝纤维化具有重要调节作用 ,并对血吸虫感染具有一定的协同免疫力。现将近年来 IL- 12抗血吸虫作用的研究进展综述如下。1　对虫卵肉芽肿形成和纤维化的调节作用血吸虫病的主要病理损害是宿主对沉积于肝脏、结肠等器官内的血…     

Treg/Th17平衡与血吸虫感染免疫

血吸虫感染可诱导调节性T细胞（Treg）和Th17型免疫反应。研究表明,Treg和Th17细胞及其平衡在血吸虫感染中具有非常重要的作用。Treg细胞抑制宿主体内过度病理反应,并有助于血吸虫逃避宿主的免疫攻击;而Th17细胞促进血吸虫感染过程中的免疫病理发展。本文就Treg/Th17平衡与血吸虫感染免疫关系的研究进展作一综述。     

血吸虫感染致Thl／Th2效应选择及其抗感染作用的分子机制

血吸虫感染导致宿主体内CD4 T细胞的高度极化反应，产生优势的Thl或Th2功能亚群，分泌不同的细胞因子，分别介导细胞免疫和体液免疫，在宿主的抗感染保护性免疫中发挥重要作用，这对血吸虫疫苗的研制具有重要的指导意义。而血吸虫感染动物模型为Thl和Th2极化的免疫效应研究提供了特异而有效的研究工具。     

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。     

血吸虫免疫逃避机制的研究现状

血吸虫免疫逃避机制是血吸虫抵抗宿主而得以存活的重要因素,目前较肯定的机制主要是抗原改变和免疫调节.抗原改变主要是血吸虫抗原的变异、模拟和伪装,使宿主的免疫临视功能敏感度下降;免疫调节主要是血吸虫通过合成神经分子、蛋白酶、细胞因子及其他小分子物质,阻断宿主补体的激活,抑制宿主的免疫细胞功能,从而下调宿主的免疫功能,这两种机制均有利于血吸虫在宿主体内的存活.     

血吸虫病因减弱巨噬细胞对硕大利什曼原虫杀伤作用而延迟其病变的消退

曼氏血吸虫 (S .mansoni)感染会延迟硕大利什曼原虫 (L .major)感染后的皮肤病变并使虫血症 ( parasitaemia)消退 ,而硕大利什曼原虫感染却未见有对血吸虫病进程的改变作用。本文旨在预先存在一个强Th2应答的感染情况下 ,研究机体对诱导Th1应答的病原体的免疫应答的改变。硕大利什曼原虫感染导致局部皮肤病变 ,其消退依赖于强烈的Th1应答的进程 ,而曼氏血吸虫感染肝脏和肠道诱导感染部位强Th2应答对宿主的存活至关重要。用曼氏血吸虫感染小鼠 2周后再用硕大利什曼原虫感染。由于对血吸虫卵的免疫应答出现在感染后 6至 7周 ,预先感染曼氏…     

烟曲霉感染中Th17免疫应答的作用机制

侵袭性肺曲霉病是一种多见的真菌感染性疾病,感染时可激活体内的固有免疫及适应性免疫以清除病原菌,起到宿主免疫保护作用.免疫细胞Th17是近年来研究热点,其主要参与免疫性疾病的免疫应答,在宿主免疫保护中起重要作用.近年来关于Th17细胞在烟曲霉感染中相关作用的研究逐渐增多,本文就烟曲霉感染时宿主的免疫应答机制的最新进展进行综述.     

Th1/Th2极化相关因子在血吸虫病肝纤维化发生发展中的作用

血吸虫病肝纤维化是宿主感染血吸虫后发生免疫反应导致的严重病理损害。宿主处于何种免疫应答状态决定了肝纤维化的进展。当宿主体内以Th1免疫应答为主时,不易发生肝纤维化;而宿主体内以Th2免疫应答为主时,易形成肝纤维化。细胞因子及共刺激分子在Th1/Th2极化过程中均发挥重要的作用。本文综述了细胞因子和共刺激分子调控Th1/Th2极化的作用及其与血吸虫病肝纤维化发生、发展相关性的研究进展。     

Toll-like receptors and T-helper-1/T-helper-2 responses

PURPOSE OF REVIEW: Toll-like receptors (TLRs) are a family of pattern recognition receptors that are activated by specific components of microbes and certain host molecules. They constitute the first line of defense against many pathogens and play a crucial role in the function of the innate immune system. Recently, TLRs were observed to influence the development of adaptive immune responses, presumably by activating antigen-presenting cells. This has important implications for our understanding of how the host tailors its immune response as a function of specific pathogen recognition. The present review discusses the recent studies that demonstrate the role of TLRs in the regulation of adaptive T-helper-1 (Th1) and Th2 responses, and the mechanisms by which the effects are carried out. RECENT FINDINGS: Most studies have focused on the role of TLRs and components of their signaling pathways in the control of Th1-type immune responses, and on the implications for their use as antimicrobial agents, such as adjuvants in vaccines, or to treat or prevent the Th2-type dominated immune responses seen in allergies. TLR-deficient mice have been described and used to come to these conclusions. Although controversial, there is also evidence that TLRs may be important for Th2-type responses, possibly by augmenting the overall maturity of dendritic cells. SUMMARY: A greater understanding of the processes by which TLRs regulate adaptive immunity may yield not only improved ways to treat infectious diseases but also new approaches to the treatment and prevention of allergic and certain autoimmune disorders.     

钩虫感染诱导宿主免疫反应及其潜在治疗价值研究进展

钩虫病是影响人类健康的全球性公共卫生问题之一,尤其在热带及亚热带地区,人群钩虫感染较为普遍。近年来,随着寄生虫感染免疫学研究的不断深入,发现钩虫等蠕虫感染引起的宿主免疫应答作用的“双向性”日益凸显：一方面诱导宿主产生杀伤感染蠕虫的免疫应答;另一方面也会引起宿主产生一系列有利于维持寄生虫寄生的免疫学改变,即通过多种复杂机制调控宿主免疫状态,导致感染宿主过敏性及自身免疫性疾病的发病减少或症状减轻,这为此类疾病的干预提供了新的思路。本文对钩虫感染后宿主免疫应答,及其对过敏性哮喘、炎症性肠病及类风湿性关节炎等疾病的潜在治疗价值研究进展进行综述。     

钩虫感染诱导宿主免疫反应及其潜在治疗价值研究进展

钩虫病是影响人类健康的全球性公共卫生问题之一，尤其在热带及亚热带地区，人群钩虫感染较为普遍。近年来，随着寄生虫感染免疫学研究的不断深入，发现钩虫等蠕虫感染引起的宿主免疫应答作用的“双向性”日益凸显：一方面诱导宿主产生杀伤感染蠕虫的免疫应答；另一方面也会引起宿主产生一系列有利于维持寄生虫寄生的免疫学改变，即通过多种复杂机制调控宿主免疫状态，导致感染宿主过敏性及自身免疫性疾病的发病减少或症状减轻，这为此类疾病的干预提供了新的思路。本文对钩虫感染后宿主免疫应答，及其对过敏性哮喘、炎症性肠病及类风湿性关节炎等疾病的潜在治疗价值研究进展进行综述。     

Emerging Role of Human Basophil Biology in Health and Disease

Basophils have emerged in recent years as a small but potent subpopulation of leukocytes capable of bridging innate and adaptive immunity. They can be activated through IgE-dependent and IgE-independent mechanisms to release preformed mediators and to produce Th2 cytokines. In addition to their role in protective immunity to helminths, basophils are major participants in allergic reactions as diverse as anaphylaxis and immediate hypersensitivity reactions, late-phase hypersensitivity reactions, and delayed hypersensitivity reactions. Additionally, basophils have been implicated in the pathophysiology of autoimmune diseases such as lupus nephritis and rheumatoid arthritis, and the modulation of immune responses to bacterial infections, as well as being a feature of myelogenous leukemias. Distinct signals for activation, degranulation, transendothelial migration, and immune regulation are being defined, and demonstrate the important role of basophils in promoting a Th2 microenvironment. These mechanistic insights are driving innovative approaches for diagnostic testing and therapeutic targeting of basophils.     

Helminth Infection and Type 1 Diabetes

The increasing incidence of type 1 diabetes (T1D) and autoimmune diseases in industrialized countries cannot be exclusively explained by genetic factors. Human epidemiological studies and animal experimental data provide accumulating evidence for the role of environmental factors, such as infections, in the regulation of allergy and autoimmune diseases. The hygiene hypothesis has formally provided a rationale for these observations, suggesting that our co-evolution with pathogens has contributed to the shaping of the present-day human immune system. Therefore, improved sanitation, together with infection control, has removed immunoregulatory mechanisms on which our immune system may depend. Helminths are multicellular organisms that have developed a wide range of strategies to manipulate the host immune system to survive and complete their reproductive cycles successfully. Immunity to helminths involves profound changes in both the innate and adaptive immune compartments, which can have a protective effect in inflammation and autoimmunity. Recently, helminth-derived antigens and molecules have been tested in vitro and in vivo to explore possible applications in the treatment of inflammatory and autoimmune diseases, including T1D. This exciting approach presents numerous challenges that will need to be addressed before it can reach safe clinical application. This review outlines basic insight into the ability of helminths to modulate the onset and progression of T1D, and frames some of the challenges that helminth-derived therapies may face in the context of clinical translation.     

Research advances of vasoactive intestinal peptide in the pathogenesis of ulcerative colitis by regulating interleukin-10 expression in regulatory B cells

Ulcerative colitis (UC) is a chronic relapsed intestinal disease with an increasing incidence around the world. The pathophysiology of UC remains unclear. However, the role of the interaction between the enteric nervous system and the immune system in the pathogenesis of UC has been the focus of attention and has become a research hotspot. Vasoactive intestinal peptide (VIP) is a kind of endogenous neuropeptide with regulatory activity on intestinal immunity. It has been shown to regulate immune disorders in animal and human experiments and has become an effective anti-inflammatory and immune modulator that affects the innate immune system and adaptive immune system. Regulatory B cells (Bregs) are a new group of B cells that negatively regulate the immunity and have received extensive attention in immune circles. Bregs can regulate immune tolerance by producing interleukin (IL)-10, IL-35, and transforming growth factor-β, suppressing autoimmune diseases or excessive inflammatory responses. The secretion of IL-10 by Bregs induces the development of T helper (Th) 0 and Th2 cells. It also induces Th2 cytokines and inhibits Th1 cytokines, thereby inhibiting Th1 cells and the Th1/Th2 balance. With further clarity on the mechanism of the regulation of IL-10 expression by VIP in Bregs in colitis patients, we believe that Bregs can provide a novel strategy for the clinical treatment of UC. Thus, we aim to review the current literature on this evolving topic.     

The Role of Complement in the Diagnosis and Management of Allergic Rhinitis and Allergic Asthma

Allergic rhinitis and asthma are common chronic inflammatory diseases of the nasal mucus membranes and the upper airways with a high prevalence in Western countries. In addition to maladaptive T-helper type 2 (Th2) immunity, Th17 cells can drive the inflammatory responses in both diseases. Several reports have shown that the complement system is activated locally and systemically in allergic rhinitis and/or allergic asthma patients. Importantly, recent findings in experimental models of allergic rhinitis and allergic asthma suggest that the complement cleavage products complement 3a and complement 5a and the activation of their corresponding receptors in antigen-presenting cells regulate the development of maladaptive Th2 and Th17 immunity. These findings in experimental asthma are corroborated by genome-wide searches and candidate gene studies in humans. We discuss recent findings in experimental and human allergic airway diseases suggesting that complement may serve as a new diagnostic and therapeutic target for both disorders.     

T辅助细胞17与气道变态反应性疾病

T辅助细胞17（helper T17,Th17）是近年来新发现的独立的辅助T细胞亚群,以分泌白细胞介素17（intedeukin17,IL-17）为主要特征。现已证实Th17在自身免疫性疾病及感染等中发挥着重要的作用。随着对Th17细胞分化及调节的深入研究,人们发现其在以Th2主导的变态反应性疾病中也扮演着重要的角色。     

Th17 and allergy.

The identification of novel helper T (Th) cell subsets, i.e., IL-17-producing Th cells (Th17 cells) and regulatory T cells (Treg cells), provided new insight into our understanding of the molecular mechanisms involved in the development of infectious and autoimmune diseases as well as immune responses, and thus led to revision of the classic Th1/Th2 paradigm. Several current lines of evidence from gene-deficient mice indicate that IL-17 and Th17 cells, but not IFN-gamma and Th1 cells, are responsible for the development of autoimmune diseases such as murine arthritis and encephalomyelitis, which have classically been considered to be Th1-mediated disorders. Th17 cells may also contribute to the pathogenesis of classically recognized Th2-mediated allergic disorders. In this review, we summarize the current knowledge regarding IL-17 and Th17 cells and discuss their potential roles in the pathogenesis of allergic disorders.     

Inflammation and immune response in atherosclerosis

Atherosclerosis is an inflammatory disease with a significant autoimmune component. Studies using transgenic murine models have clarified that recruitment of mononuclear leukocytes through vascular leukocyte-adhesion molecules and chemokines, differentiation of monocytes to macrophages, and endocytosis through scavenger receptors all are of decisive importance for atherosclerosis in hypercholesterolemic mice. T and B cells modulate disease progression and lesion development is reduced in mice lacking adaptive immunity. In particular, local immune responses eliciting Th1 effector mechanisms appear to be proatherogenic, whereas protective immune responses can be induced by immunization with oxidized low-density lipoprotein. Thus, innate immunity is necessary for atherosclerosis, whereas adaptive immunity is an important modulator of disease development.