宿主甲状腺素和白介素-7水平的早期变化对曼氏血吸虫发育的影响

血吸虫通过钻入皮肤而感染脊椎动物宿主,诱导皮肤产生白介素 7(IL 7)。IL 7在血吸虫的移行、发育、成熟及对宿主的损害中都是必需的。在IL 7缺陷小鼠感染血吸虫后,虫体虽然出现性别分化,但发育较小。在甲状腺机能低下小鼠中也有类似报道,而在甲状腺机能亢进小鼠中,血吸虫发育肥大,成熟较早,产卵量大。激素是直接影响血吸虫的发育,还是通过调节宿主对血吸虫的免疫应答而影响其发育目前尚不清楚。T4是甲状腺中合成甲状腺素(THs)的主要形式,在肝、肾等组织中活化为T3。T3和T4参与B和T淋巴细胞、NK细胞的发育增殖和功能分化。在TH和IL 7…     

血吸虫发育中的激素和核受体

本文综述了血吸虫宿主类固醇、甲状腺分泌的激素对血吸虫发育的影响,从种系发生学角度分析核受体超家族,并且对最早发现的血吸虫核受体进行鉴定,结果表明甲状腺分泌的激素对血吸虫的作用是间接的,不涉及基因转录。血吸虫体内核受体的存在,为开发药靶提供了可能性。     

血吸虫发育中的激素和核受体

本综述了血吸虫宿主类固醇、甲状腺分泌的激素对血吸虫发育的影响，从种系发生学角度分析核受体超家族，并且对最早发现的血吸虫核受体进行鉴定，结果表明甲状腺分泌的激素对血吸虫的作用是间接的，不涉及基因转录，血吸虫体内核受体的存在，为开发药靶提供了可能性。     

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.     

一种可能参与寄生虫内部及宿主与寄生虫信号的曼氏血吸虫脑啡肽能系统

曼氏血吸虫逃避,或至少部分逃避中间宿主及终宿主的免疫应答。近几年,作者对血吸虫在免疫逃避中神经多肽的参与进行了研究。经放射免疫分析发现,在曼氏血吸虫毛蚴、尾蚴、童虫和成虫各期,都有与促肾上腺皮质素、促黑素细胞激素及β-内啡肽相关的分子。还发现在不同生活阶段,这些生物活性多肽被释放并影响宿主的免疫应答,表明血吸虫和宿主能通过这些它们共有的信号     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

血吸虫感染诱导免疫偏移的研究进展

近年来,包括血吸虫在内的蠕虫诱导宿主免疫偏移日益成为研究的热点.该文综述血吸虫感染诱导免疫偏移的研究及进展,包括对血吸虫感染诱导宿主免疫细胞的作用、细胞因子以及信号转导通路及其对自身免疫性疾病的负向调控作用进行了介绍.     

血吸虫蛋白水解酶的研究进展

血吸虫通过分解宿主血红蛋白获得生长、发育和繁殖所需的氨基酸。一系列的血吸虫 蛋白水解酶参与了宿主血红蛋白的降解过程。本文综述了近年血吸虫组织蛋白酶B、L、D,血吸虫 豆酶及二肽酶系等方面的研究进展。     

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。     

血吸虫细胞凋亡研究进展

细胞凋亡对血吸虫及各种生物体的生长、发育具有重要的作用。近年来,一些学者在血吸虫的细胞凋亡现象观察、凋亡在血吸虫生长发育中的作用方面开展了探索,以寻找、开拓防治血吸虫病的新途径,为控制血吸虫病的传播提供新思路。该文对有关血吸虫细胞凋亡、血吸虫与宿主细胞凋亡现象、血吸虫重要凋亡基因的相关研究及血吸虫细胞凋亡研究的应用前景作一简述。     

Schistosome glycans and innate immunity

Schistosome glycans induce characteristic innate immune responses in the infected host. The molecular aspects of these responses, the pathways and receptors as well as the schistosome glycans and glycoconjugates involved, form an area of intense research. The relevant schistosome glycan elements and the possible mechanisms through which they act on the innate immune system are discussed in this review.     

Cytokines in the liver

Cytokines comprise a group of small proteins released from cells in order to influence the function of other cells. By binding to highly specific cell-surface receptors, they trigger a vast array of intracellular signalling cascades. Cytokines have been described as interleukins, growth factors, interferons and chemokines. Unlike hormones, which act in a similar way, cytokines are produced by many different types of cell and act on many other types. Most of them are produced only after certain stimuli. The most intense field of cytokine activity is without doubt host defence.The liver resembles a central organ of cytokine activity due to the fact that it hosts hepatocytes, which are highly susceptible to the activity of cytokines in a variety of physiological and pathophysiological processes. Moreover, the non-parenchymal cells of the liver, in particular Kupffer cells (KCs), the resident tissue macrophages of the liver, are able to synthesize a variety of cytokines that may act systemically on any other organ of the body, or in a paracrine manner on hepatocytes and other non-parenchymal liver cells. A classic example of how cytokines act can be observed during the acute phase reaction discussed in this article. The role of cytokines in liver development, acute liver injury, liver regeneration, liver fibrosis and liver metastasis is also discussed.     

Infection, immunity, and hormones/endocrine interactions

Infections and stress, immune responses, and hormones are interconnected, ensuring immune competence to deal with immediate threat of overwhelming infection and metabolic collapse. Emergence of cytokines as key signal mediators and appreciation of autocrine-paracrine influences of hormones have helped explain how signals are transmitted and responses evoked. This has led to possibilities of creating therapies that might be used to enhance protective signals and dampen signals emanating from host and invading organism interaction that might otherwise be detrimental. Correcting certain metabolic abnormalities, such as hyperglycemia and metabolic acidosis, benefits the host by decreasing morbidity and mortality.     

Mammary developmental fate and breast cancer risk

The ovarian hormones, estrogen and progesterone, play a pivotal role in normal and neoplastic development of the mammary gland. These hormones have a paradoxical role as long duration of estrogen and progesterone are associated with increased breast cancer risk, while short duration of pregnancy level doses are associated with a reduced breast cancer risk. The protective effects of estrogen and progesterone, as well as pregnancy, have been extensively studied in animal models. Recent studies have demonstrated that these hormones induce alterations in gene expression in the mammary epithelial cells which persist for a long time after the hormones are withdrawn from the host. It is postulated that hormones induce a switch in mammary developmental fate which decreases the risk of breast cancer over the lifetime of the host. Some of the possible cellular pathways persistently altered by short term hormone exposure are a decrease in growth factors and an increase in apoptosis. The expression of these genes, in turn, may be affected by alterations in genes regulating chromatin remodeling. The relative contributions of host-mediated factors and mammary cell intrinsic factors remain to be determined. The current studies have moved this research area from the biological to the molecular realm and offer the potential for directing prevention efforts at specific molecular targets.     

Hepatitis-related hepatocellular carcinoma: Insights into cytokine gene polymorphisms

Hepatocellular carcinoma(HCC) is a primary liver cancer, which is one of the most prevalent cancers among humans. Many factors are involved in the liver carcinogenesis as lifestyle and environmental factors. Hepatitis virus infections are now recognized as the chief etiology of HCC; however, the precise mechanism is still enigmatic till now. The inflammation triggered by the cytokine-mediated immune response, was reported to be the closest factor of HCC development. Cytokines are immunoregulatory proteins produced by immune cells, functioning as orchestrators of the immune response. Genes of cytokines and their receptors are known to be polymorphic, which give rise to variations in their genes. These variations have a great impact on the expression levels of the secreted cytokines. Therefore, cytokine gene polymorphisms are involved in the molecular mechanisms of several diseases. This piece of work aims to shed much light on the role of cytokine gene polymorphisms as genetic host factor in hepatitis related HCC.     

Molluscan and vertebrate immune responses to bird schistosomes

There is a growing understanding of risks posed by human contact with the cercariae of bird schistosomes. In general, there are no fundamental biological differences between human and bird schistosomes in terms of their interactions with snail and vertebrate hosts. The penetration of host surfaces is accompanied by the release of penetration gland products and the shedding of highly antigenic surface components (miracidial ciliated plates and cercarial glycocalyx) which trigger host immune reactions. New surface structures are formed during transformation: the tegument of mother sporocysts and the tegumental double membrane of schistosomula. These surfaces apparently serve as protection against the host immune response. Certain parasite excretory-secretory products may contribute to immunosuppression or, on the other hand, stimulation of host immune reactions. Discovery of new species and their life cycles, the characterization of host-parasite interactions (including at the molecular level), the determination of parasite pathogenicity towards the host, the development of tools for differential diagnosis and the application of protective measures are all topical research streams of the future. Regularly updated information on bird schistosomes and cercarial dermatitis can be found at http://www.schistosomes.cz (web pages of Schistosome Group Prague).     

结核病免疫学研究进展

机体的免疫系统是复杂精细的动态平衡系统,结核病的感染、发生、发展及转归与机体免疫系统变化密切相关,细胞免疫是主要的保护性免疫,其免疫调节作用是通过亚群细胞实现的,其中CD4-和CD8-T细胞在抵抗结核分枝杆菌感染中有重要作用.但免疫细胞间的相互作用不是孤立的,多种细胞因子参与其中,细胞因子的释放直接影响免疫应答的结果....     

Factors for the onset of and the exacerbation of tuberculosis. 2. Host factors promoting the occurrence and exacerbation of tuberculosis: significance of Th1-Th2 cytokine balance

The problem of tuberculosis is emerging again with increase in the population of aged people and immunocompromised patients in Japan. It has been well documented that cell-mediated immunity play a central role in host resistance to infection with Mycobacterium tuberculosis. A decade years ago, Mosmann et al. found that helper T (Th) cells are divided into two subsets, Th1 and Th2, based on the cytokines which they produce. Th1 cells produce IFN-gamma, while Th2 cells secrete IL-4, IL-10 and IL-13. Many recent studies have provided evidences suggesting that the Th1-Th2 cytokine balance may determine the outcome of some diseases. For example, predominant production of Th1 cytokines may prevent the occurrence of infectious diseases caused by intracellularly growing pathogens and Th2 cytokines may be involved in the exacerbation of allergic diseases. On the other hand, IL-12 plays an essential role in the differentiation of Th1 cells from naive T cells, and IL-18 potentiates this effect although it does not show such effect by itself. In the present study, we examined the role for these two cytokines in host resistance to mycobacterial infection by using an animal model with either IL-12 or IL-18 gene-disrupted mice. The organ loads of this pathogen in lung, liver and spleen were significantly larger in these gene-disrupted mice than those in control mice. There are several host factors which determines the outcome of mycobacterial infection. Among them, steroid treatment and AIDS are important factors. In this study, we determined the effect of these pathological conditions on Th1-Th2 cytokine balance and outcome of mycobacterial infection using murine models. In both conditions, the exacerbated infection was well correlated with the reduced production of IFN-gamma. Furthermore, I also discussed about the relationship between other host factors and balance in the production of Th1 and Th2 cytokines.     

血吸虫尾蚴侵染分子机制研究进展

尾蚴穿透宿主皮肤是血吸虫成功感染终宿主的第一步。尾蚴钻腺分泌的蛋白酶在穿透宿主皮肤过程中发挥了 重要作用。目前对于血吸虫感染分子机制的研究主要集中在包括丝氨酸蛋白酶和半胱氨酸蛋白酶在内的尾蚴分泌蛋白 酶上。已有研究表明, 曼氏血吸虫主要靠尾蚴分泌的弹性蛋白酶穿透宿主皮肤, 日本血吸虫则主要利用组织蛋白酶B2侵 入宿主体内。尾蚴入侵分子机制的阐明有助于新型血吸虫病疫苗的研制和药物靶点的发现。