浅谈细胞因子网络性

细胞因子是在机体炎症和免疫应答中 ,由免疫细胞产生的一类具有调节与效应功能的小分子多肽或蛋白。它作为细胞间的信号在免疫应答中起作用。细胞因子在非特异性免疫中称单核因子 ,在特异性免疫中又可叫淋巴因子。细胞因子根据其功能的不同可分好多种 ,但不同的细胞因子并不是单一存在 ,它们互相之间相辅相成 ,共同作用 ,使机体处于一个相对稳定的状态。本文即从细胞因子的产生、功能、受体类型等方面论述细胞因子的网络性     

泌乳素与免疫系统功能关系的研究

泌乳素主要由垂体前叶细胞分泌，属经典的神经分泌激素，其能以内分泌的形式作用于远端的靶器官，并发挥生物学效应。近年来发现，许多免疫细胞亦可以产生泌乳素，并且作为一种调节性的前炎性因子，通过与免疫细胞表面的泌乳素受体结合，实现对机体免疫应答的调节。本文对泌乳素与免疫系统、免疫细胞、细胞因子之间的相互作用关系以及其在免疫细胞中的信号传导途径做一综述。     

白细胞介素-1的结构、来源、分布、功能及其与疾病的关系

白细胞介素-1(IL-1)不仅作为一种重要的细胞因子,是体内调节免疫和炎症反应的中心介质,而且它也作为神经递质或生长因子参与了机体多个系统的病理生理活动,其生物学作用非常广泛.近年来,随着对神经系统、免疫系统和内分泌系统之间相互作用研究的日益深入,IL-1在各系统中的作用与机制也得到了相应的证实,并为一些临床疾病的诊治提供了有力依据.文章针对IL-1作为脑源性白介素在中枢神经系统的病理生理功能进行了研究.     

神经免疫调节相关脑区的研究进展

脑和免疫系统具有双向的相互调节作用。脑可以通过HPA轴和对免疫器官的直接神经支配来调节外周免疫功能;外周免疫活动的信息同样可由神经和体液的途径传入脑,如免疫细胞通过激活传入迷走神经或分泌细胞因子来影响中枢神经元的活动。大脑皮层、基底前脑、中脑和脑干中的许多结构都与免疫有关,尤其下丘脑和边缘系统作为神经内分泌和自主神经系统的调控中心,组成神经免疫调节的重要解剖基础。     

体育运动全球化思考

本文以体育运动发展历史、体育的全球化现象和体育文化这三者之间的关系为切入点，思考它们之间存在的哲学关系，以期为体育运动全球化过程中外来体育运动和本区域体育运动之间的互动、融合提供思考方向。     

体育运动全球化思考

本文以体育运动发展历史、体育的全球化现象和体育文化这三者之间的关系为切入点,思考它们之间存在的哲学关系,以期为体育运动全球化过程中外来体育运动和本区域体育运动之间的互动、融合提供思考方向。     

乳酸杆菌通过定植和提供免疫信号调节宿主免疫反应

提取了Lactobacillussp.的肽聚糖,用AffymetrixMOE430A基因芯片研究了肽聚糖对机体免疫细胞基因表达的影响。结果发现,乳酸杆菌肽聚糖可以刺激免疫细胞Th1型免疫反应相关基因的表达,可能激活TLR-NF-κB相关信号通路,同时,不同剂量的肽聚糖可能通过调节Tollip的表达,影响TLR-NF-κB信号通路的激活,从而调节细胞因子的表达。     

免疫系统对家畜生殖功能的调节和影响（综述）

免疫系统及其由免疫细胞产生的生物活性蛋白或类脂与大多数生殖细胞的产生复杂的网络交互作用，从而调节神经内分泌和生殖功能。本文从免疫系统与生殖道，输精的免疫反应，细胞因子的作用及免疫系统与生殖腺的功能，与妊娠，泌乳以及公母畜不孕方面综述了近年的研究文献。     

瑜伽与体育舞蹈在高校阳光体育运动中的价值研究

瑜伽和体育舞蹈都是新兴的体育运动项目，它们以强烈的娱乐、竞技、表演和浓郁的艺术色彩，深受当代大学生的喜爱。结合“阳光体育运动”的全面实施，系统地阐述了瑜伽和体育舞蹈的内涵及技术特征，从而深入探讨这两个运动项目在高校阳光体育运动中的价值，旨在促进它们在高校阳光体育运动中得以普及和广泛开展。     

细胞因子在骨质疏松症发病机理中的作用及运动对其的影响

骨质疏松症的发病机理与细胞因子改变有密切的关系。部分细胞因子表达增加或降低会影响骨的微环境中细胞的增殖,分化,使骨形成与骨吸收之间发生紊乱,骨代谢偶联失衡,从而导致骨质疏松症的发生。体育运动可以改变体内细胞因子的表达,从而起到防治骨质疏松症的作用。     

A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera

Myeloproliferative disorders are clonal haematopoietic stem cell malignancies characterized by independency or hypersensitivity of haematopoietic progenitors to numerous cytokines. The molecular basis of most myeloproliferative disorders is unknown. On the basis of the model of chronic myeloid leukaemia, it is expected that a constitutive tyrosine kinase activity could be at the origin of these diseases. Polycythaemia vera is an acquired myeloproliferative disorder, characterized by the presence of polycythaemia diversely associated with thrombocytosis, leukocytosis and splenomegaly. Polycythaemia vera progenitors are hypersensitive to erythropoietin and other cytokines. Here, we describe a clonal and recurrent mutation in the JH2 pseudo-kinase domain of the Janus kinase 2 (JAK2) gene in most (> 80%) polycythaemia vera patients. The mutation, a valine-to-phenylalanine substitution at amino acid position 617, leads to constitutive tyrosine phosphorylation activity that promotes cytokine hypersensitivity and induces erythrocytosis in a mouse model. As this mutation is also found in other myeloproliferative disorders, this unique mutation will permit a new molecular classification of these disorders and novel therapeutical approaches.     

Rapid on/off cycling of cytokine production by virus-specific CD8+ T cells.

CD8-positive T cells protect the body against viral pathogens by two important mechanisms: production of antiviral cytokines and lysis of infected cells. Cytokine production can have both local and systemic consequences, whereas cytolytic activity is limited to infected cells that are in direct contact with T cells. Here we analyse activated CD8-positive T cells from mice infected with lymphocytic choriomeningitis virus and find that cytokines are not produced ex vivo in the absence of peptide stimulation, but that they are rapidly generated after T cells encounter viral peptides bound to the major histocompatibility complex. Remarkably, cytokine production ceases immediately upon dissociation of the T cells from their targets and resumes when antigenic contact is restored. In contrast to the 'on/off/on' cycling of cytokines, the pore-forming cytotoxic protein perforin is constitutively maintained. Our results indicate that there is differential expression of effector molecules according to whether the antiviral product is secreted (like cytokines) or stored inside the cell (like perforin). The ability to turn cytokines on and off while maintaining intracellular stores of perforin shows the versatility of the cellular immune response and provides a mechanism for maintaining effective immune surveillance while reducing systemic immunopathology.     

Development of Th1-type immune responses requires the type I cytokine receptor TCCR

On antigen challenge, T-helper cells differentiate into two functionally distinct subsets, Th1 and Th2, characterized by the different effector cytokines that they secrete. Th1 cells produce interleukin (IL)-2, interferon-gamma (IFN-gamma) and lymphotoxin-beta, which mediate pro-inflammatory functions critical for the development of cell-mediated immune responses, whereas Th2 cells secrete cytokines such as IL-4, IL-5 and IL-10 that enhance humoral immunity. This process of T-helper cell differentiation is tightly regulated by cytokines. Here we report a new member of the type I cytokine receptor family, designated T-cell cytokine receptor (TCCR). When challenged in vivo with protein antigen, TCCR-deficient mice had impaired Th1 response as measured by IFN-gamma production. TCCR-deficient mice also had increased susceptibility to infection with an intracellular pathogen, Listeria monocytogenes. In addition, levels of antigen-specific immunoglobulin-gamma2a, which are dependent on Th1 cells, were markedly reduced in these mice. Our results demonstrate the existence of a new cytokine receptor involved in regulating the adaptive immune response and critical to the generation of a Th1 response.     

Cell-fate conversion of lymphoid-committed progenitors by instructive actions of cytokines

The primary role of cytokines in haemato-lymphopoiesis is thought to be the regulation of cell growth and survival. But the instructive action of cytokines in haematopoiesis has not been well addressed. Here we show that a clonogenic common lymphoid progenitor, a bone marrow-resident cell that gives rise exclusively to lymphocytes (T, B and natural killer cells), can be redirected to the myeloid lineage by stimulation through exogenously expressed interleukin (IL)-2 and GM-CSF (granulocyte/macrophage colony-stimulating factor) receptors. Analysis of mutants of the beta-chain of the IL-2 receptor revealed that the granulocyte- and monocyte-differentiation signals are triggered by different cytoplasmic domains, showing that the signalling pathway(s) responsible for these unique developmental outcomes are separable. Finally, we show that the endogenous myelomonocytic cytokine receptors for GM-CSF and macrophage colony-stimulating factor (M-CSF) are expressed at low to moderate levels on the more primitive haematopoietic stem cells, are absent on common lymphoid progenitors, and are upregulated after myeloid lineage induction by IL-2. We conclude that cytokine signalling can regulate cell-fate decisions and propose that a critical step in lymphoid commitment is downregulation of cytokine receptors that drive myeloid cell development.     

Human large granular lymphocytes are potent producers of interleukin-1

Natural killer (NK) activity against tumour and virus-infected target cells is shown by a subpopulation of peripheral blood mononuclear leukocytes with the morphological features of large granular lymphocytes (LGL). The lineage of human LGL is still controversial, as they display surface markers of both T lymphocytes and myelomonocytic cells. LGL have recently been reported to produce lymphokines such as interleukin-2 (IL-2) and alpha- as well as gamma-interferons, functions associated mainly with T cells. To determine whether cytokines associated with other cell lineages are also produced by LGL, we examined whether they might produce a myelomonocyte -associated cytokine such as interleukin-1 (IL-1). IL-1 is a 12-18,000 molecular weight (MW) lymphokine produced by a variety of cell types such as monocytes, keratinocytes and a human dendritic cell line, which plays a crucial role in immunoregulation and inflammation. Moreover, IL-1 has recently been reported to act synergistically with IL-2 and interferons in boosting LGL-mediated NK activity. We now show that a subset of highly purified human LGL with NK activity can be stimulated to secrete a soluble factor with the biochemical and biological characteristics of human IL-1.     

白细胞介素-10与支气管哮喘之间关系的研究

白细胞介素-10(IL-10)主要由ThO和Th2细胞在激活状态下分泌的一种细胞因子,是具有多向性生物活性的强力免疫抑制因子,可阻断多种炎性细胞因子的合成,具有抗炎作用,文章就其与支气管哮喘之间关系的研究进展作一报道.     

Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin

Vertebrates achieve internal homeostasis during infection or injury by balancing the activities of proinflammatory and anti-inflammatory pathways. Endotoxin (lipopolysaccharide), produced by all gram-negative bacteria, activates macrophages to release cytokines that are potentially lethal. The central nervous system regulates systemic inflammatory responses to endotoxin through humoral mechanisms. Activation of afferent vagus nerve fibres by endotoxin or cytokines stimulates hypothalamic-pituitary-adrenal anti-inflammatory responses. However, comparatively little is known about the role of efferent vagus nerve signalling in modulating inflammation. Here, we describe a previously unrecognized, parasympathetic anti-inflammatory pathway by which the brain modulates systemic inflammatory responses to endotoxin. Acetylcholine, the principle vagal neurotransmitter, significantly attenuated the release of cytokines (tumour necrosis factor (TNF), interleukin (IL)-1beta, IL-6 and IL-18), but not the anti-inflammatory cytokine IL-10, in lipopolysaccharide-stimulated human macrophage cultures. Direct electrical stimulation of the peripheral vagus nerve in vivo during lethal endotoxaemia in rats inhibited TNF synthesis in liver, attenuated peak serum TNF amounts, and prevented the development of shock.     

Interchromosomal associations between alternatively expressed loci

The T-helper-cell 1 and 2 (T(H)1 and T(H)2) pathways, defined by cytokines interferon-gamma (IFN-gamma) and interleukin-4 (IL-4), respectively, comprise two alternative CD4+ T-cell fates, with functional consequences for the host immune system. These cytokine genes are encoded on different chromosomes. The recently described T(H)2 locus control region (LCR) coordinately regulates the T(H)2 cytokine genes by participating in a complex between the LCR and promoters of the cytokine genes Il4, Il5 and Il13. Although they are spread over 120 kilobases, these elements are closely juxtaposed in the nucleus in a poised chromatin conformation. In addition to these intrachromosomal interactions, we now describe interchromosomal interactions between the promoter region of the IFN-gamma gene on chromosome 10 and the regulatory regions of the T(H)2 cytokine locus on chromosome 11. DNase I hypersensitive sites that comprise the T(H)2 LCR developmentally regulate these interchromosomal interactions. Furthermore, there seems to be a cell-type-specific dynamic interaction between interacting chromatin partners whereby interchromosomal interactions are apparently lost in favour of intrachromosomal ones upon gene activation. Thus, we provide an example of eukaryotic genes located on separate chromosomes associating physically in the nucleus via interactions that may have a function in coordinating gene expression.