NK细胞免疫调节功能的前沿问题--"NK-reg"是否存在

免疫系统通过识别自我和非我保护机体免受外来病原体的侵袭，同时又通过对自身抗原的免疫耐受来防止自身免疫性疾病的发生。不适当的免疫应答，如对自身抗原产生应答，对外来病原体产生免疫耐受或应答过强，均会对机体造成严重损伤。为维持机体内环境的平衡，在免疫系统进化过程中，机体形成了多方位、多层次的免疫调控体系，如细胞因子网络、抗体的独特型网络、免疫细胞间的网络调节等。     

精神神经免疫学的兴起及其研究进展

神经内分泌系统与免疫系统之间存在双向信息传递机制，即免疫系统不仅受神经、内分泌系统的调控，而且还能调节神经、内分泌系统的某些功能。这种相互作用的功能联系是通过种经、内分泌和免疫三大调节系统共有的化学信息分子与受体实现的。即：免疫系统不仅具有多种神经内分泌激素的受体，还能合成各种免疫神经递质和内分泌激素，并对其发生反应：免疫系统产生的单核细胞因子能影响中枢神经系统（ＣＮＳ），ＣＮＳ又能合成细胞因子及其受体，且对其发生反应。     

精神神经免疫学的兴起及其研究进展

神经内分泌系统与免疫系统之间存在双向信息传递机制，即免疫系统不仅受神经、内分泌系统的调控，而且还能调节神经、内分泌系统的某些功能。这种相互作用的功能联系是通过神经、内分泌和免疫三大调节系统共有的化学信息分子与受体实现的。即：免疫系统不仅具有多种神经内分泌激素的受体，还能合成各种免疫神弱递质和内分泌激素，并其发生反应；免疫系统产生的单核细胞因子能影响中枢神经系统（ＣＮＳ），ＣＮＳ又能合成细胞因子及其     

利用重组病毒表达细胞因子——一种新的疫苗策略

免疫系统可为激素样的细胞因子激活和调控,这一发现为设计重组疫苗拓开了新的机遇之门.编码细胞因子的活疫苗载体可增加病毒载体的安全性,并可操纵免疫应答以诱导出有效的保护性免疫.一、细胞因子和免疫应答细胞因子是一类参与细胞间,主要是免疫系统的细胞间互相联系的信号传递分子.它们不但可决定免疫应答的程度,还可决定其应答类型.现在看来,由传染性因子诱导的免疫力部分地由不同T淋巴细胞亚型所分泌的细胞因子类型所决定.T_(Ⅱ1)分泌IL-2     

锌指蛋自在免疫学研究中的进展

锌指结构目前已发现了10多个不同的锌指家族.锌指蛋白具有广泛的生物功能,如DNA识别,RNA包装,转录及转录后调控,蛋白折叠和装配,参与肿瘤的形成且与机体免疫系统密切相关等.本文旨在综述近年来锌指蛋白与免疫及免疫系统中的研究进展,如锌指蛋白对免疫细胞,细胞因子,免疫性疾病,肿瘤免疫及AIDS等的免疫调节.     

神经-内分泌-免疫调节网络与疾病

近年来对神经 -内分泌系统和免疫系统之间相互作用、相互依赖的复杂关系的研究已经成为一门独立的边缘学科 ,即神经免疫调节 (ｎｅｕｒｏｉｍ ｍｕｎｏｒｅｇｕｌａｔｉｏｎ)或神经免疫内分泌学[1 ] (ｎｅｕｒｏ -ｉｍ ｍｕｎｏ -ｅｎｄｏｃｒｉｎｏｌｏｇｙ)。研究者们已通过大量实验证实 ,神经系统通过其广泛的外周神经突触及其分泌的神经递质和众多的内分泌激素[2 ] ,甚至还有神经细胞分泌的细胞因子[3] ,来共同调控着免疫系统的功能 ;而免疫系统通过免疫细胞产生的多种细胞因子和激素样物质反馈作用于神经内分泌系统[4] 。两个系统的细…     

副免疫

初级免疫系统在抵抗微生物入侵的第一道防线中具有重要作用，该系统由一个相互关联、互相传递的网络调节着效应细胞对“非已”抗原产生灵活多变的应答，保证了与特异性免疫应答整个过程的密切联系。在非特异性防御水平上的免疫刺激，最初被认为是疫苗接种的副作用，实际上目前应该把用细胞因子替代的免疫系统，与模拟天然抗原而诱生的非特异性防御，即副免疫区别开来。副免疫除了在初级免疫系统以诱生短期高效的免疫作用外，还可有效     

细胞因子在神经系统相关疾病发病中的作用

免疫系统与神经系统间的相互作用机制一直是研究的热点之一,其中主要由免疫系统产生的细胞因子在免疫与神经两大系统的联系中起到了重大作用,同时在神经系统相关疾病的发病机制中起到了重要作用.本文针对细胞因子在神经系统相关疾病的发病机制中的作用进行了综述.     

NK细胞趋化因子和细胞因子的分泌与调节

NK细胞是固有免疫系统中一个非常重要的成员，能够杀死病毒、细菌、寄生虫感染的细胞以及肿瘤细胞。同时，NK细胞也可以分泌一些细胞因子和趋化因子来调节免疫应答以及炎症反应，然而，这种分泌功能与NK细胞的成熟状态相关，同时也受到一些调控因子的调节，比如P1108，深入研究这些因子的功能和调控过程，对NK细胞参与免疫应答以及炎症反应具有重要意义。     

副免疫

初级免疫系统在抵抗微生物入侵的第一道防线中具有重要作用，该系统由一个相互关联、互相传递的网络调节着效应细胞对“非已”抗原产生灵活多变的应答，保证了与特异性免疫应答整个过程的密切联系。在非特异性防御水平上的免疫刺激，最初被认为是疫苗接种的副作用，实际上目前应该把用细胞因子替代的免疫系统，与接触模拟天然抗原而诱生的非特异性防御，即副免疫（ｐａｒａｍｕｎｉｚａｔｉｏｎ）区别开来。副免疫除了在初级免疫系统能诱生短期高效的免疫作用外，还可有效地影响特异性应答。     

Bidirectional roles of skeletal muscle fibro-adipogenic progenitors in homeostasis and disease

Sarcopenia and myopathies cause progressive muscle weakness and degeneration, which are closely associated with fat infiltration and fibrosis in muscle. Recently, experimental research has shed light on fibro-adipogenic progenitors (FAPs), also known as muscle-resident mesenchymal progenitors with multiple differentiation potential for adipogenesis, fibrosis, osteogenesis and chondrogenesis. They are considered key regulators of muscle homeostasis and integrity. They play supportive roles in muscle development and repair by orchestrating the regulatory interplay between muscle stem cells (MuSCs) and immune cells. Interestingly, FAPs also contribute to intramuscular fat infiltration, fibrosis and other pathologies when the functional integrity of the network is compromised. In this review, we summarize recent insights into the roles of FAPs in maintenance of skeletal muscle homeostasis, and discuss the underlying mechanisms regulating FAPs behavior and fate, highlighting their roles in participating in efficient muscle repair and fat infiltrated muscle degeneration as well as during muscle atrophy. We suggest that controlling and predicting FAPs differentiation may become a promising strategy to improve muscle function and prevent irreparable muscle damage.     

Coordinate regulation of immune and inflammatory responses by cytokines

In response to antigenic stimulation, T cells and macrophages secrete a set of glycoproteins termed lymphokines and monokines such as IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, GM-CSF, G-CSF, IFN-alpha, IFN-gamma, TNF-alpha, and lymphotoxin. These glycoproteins mediate immune and inflammatory responses by regulating proliferation, differentiation and maturation of lymphocytes, hemopoietic cells and endothelial cells. Along with factors such as M-CSF, IL-7, LIF, IFN-beta and TGF-beta produced by stromal cells, all these molecules are collectively called cytokines. Most cytokines are pleiotropic and have multiple biological activities. Accordingly, regulatory network is formed between lymphoid cells, hemopoietic cells and endothelial cells. All or a part of this network can be activated in different ways by unique combinations of cytokines. IL-3, IL-4 and IL-5 produced by TH2 cells enhance whereas IFN-gamma produced by TH1 cells suppresses IgE mediated allergic response. Through production of a spectrum of cytokines, T cells and macrophages play a vital role in coordinating the function of different body compartments in immune and inflammatory responses. The activation of cytokines genes in T cells and macrophages is transient. Therefore, an inflammatory response that involves proliferation and maturation of hemopoietic progenitor cells may be restricted to the site of cytokine production. The inducible nature of the hemopoiesis associated with inflammatory response is in contrast to the constitutive, steady state hemopoiesis that occurs in the bone marrow microenvironment in the absence of immunological stimuli.     

Renin-angiotensin system in ventilator-induced diaphragmatic dysfunction: Potential protective role of Angiotensin (1–7)

Ventilator-induced diaphragmatic dysfunction is a feared complication of mechanical ventilation that adversely affects the outcome of intensive care patients. Human and animal studies demonstrate atrophy and ultrastructural alteration of diaphragmatic muscular fibers attributable to increased oxidative stress, depression of the anabolic pathway regulated by Insulin-like growing factor 1 and increased proteolysis. The renin-angiotensin system, through its main peptide Angiotensin II, plays a major role in skeletal muscle diseases, mainly increasing oxidative stress and inducing insulin resistance, atrophy and fibrosis. Conversely, its counter-regulatory peptide Angiotensin (1–7) has a protective role in these processes. Recent data on rodent models show that renin-angiotensin system is activated after mechanical ventilation and that infusion of Angiotensin II induces diaphragmatic skeletal muscle atrophy. Given: (A) common pathways shared by ventilator-induced diaphragmatic dysfunction and skeletal muscle pathology induced by renin-angiotensin system, (B) evidences of an involvement of renin-angiotensin system in diaphragm atrophy and dysfunction, we hypothesize that renin-angiotensin system plays an important role in ventilator-induced diaphragmatic dysfunction, while Angiotensin (1–7) can have a protective effect on this pathological process.The activation of renin-angiotensin system in ventilator-induced diaphragmatic dysfunction can be demonstrated by quantification of its main components in the diaphragm of ventilated humans or animals. The infusion of Angiotensin (1–7) in an established rodent model of ventilator-induced diaphragmatic dysfunction can be used to test its potential protective role, that can be further confirmed with the infusion of Angiotensin (1–7) antagonists like A-779. Verifying this hypothesis can help in understanding the processes involved in ventilator-induced diaphragmatic dysfunction pathophysiology and open new possibilities for its prevention and treatment.     

不同制动时相兔骨骼肌萎缩与细胞凋亡的实验研究-原位缺口末端标记法(TUNEL)的观察检测

探讨制动后骨骼肌萎缩的发生机制与骨骼肌细胞凋亡的关系。按照 Sievanen法制备不同时相的制动实验组 ,2 4只实验兔随机分为 4组 ,每组 6只 ,实验侧用管形石膏固定 ,自身未固定侧做对照组。在制动后 3、7、14和 2 8d取材 ,应用末端转移酶介导的 U TP缺口末端标记法 (Td T— mediated d UTP nick end labeling,TUNEL )检测萎缩骨骼肌中有无凋亡的骨骼肌细胞 ,并与形态学的观察结果相对照。对各组的数据进行统计学处理。结果表明不同制动时相所致的萎缩骨骼肌中均可发现有程度不一的骨骼肌细胞发生凋亡 ,以 14 d组最为显著。不同时相凋亡的肌细胞在空间的分布上呈不一致性。制动所致萎缩的骨骼肌中有时可见呈假阳性 TU NEL染色 ,但与凋亡的肌细胞的表现是不同的。我们认为 (1)制动后骨骼肌萎缩有骨骼肌细胞凋亡的参与。 (2 )骨骼肌细胞凋亡的多少与制动时相密切相关 ,以制动后 14 d最为明显。 (3)凋亡的骨骼肌细胞在空间分布上随制动时相不同而不同 ,呈不一致性。 (4 )制动后骨骼肌萎缩的程度与肌细胞凋亡的程度密切相关。     

Regenerative function of immune system: Modulation of muscle stem cells

Ageing is characterised by progressive deterioration of physiological systems and the loss of skeletal muscle mass is one of the most recognisable, leading to muscle weakness and mobility impairments. This review highlights interactions between the immune system and skeletal muscle stem cells (widely termed satellite cells or myoblasts) to influence satellite cell behaviour during muscle regeneration after injury, and outlines deficits associated with ageing. Resident neutrophils and macrophages in skeletal muscle become activated when muscle fibres are damaged via stimuli (e.g. contusions, strains, avulsions, hyperextensions, ruptures) and release high concentrations of cytokines, chemokines and growth factors into the microenvironment. These localised responses serve to attract additional immune cells which can reach in excess of 1 × 10⁵ immune cell/mm³ of skeletal muscle in order to orchestrate the repair process. T-cells have a delayed response, reaching peak activation roughly 4 days after the initial damage. The cytokines and growth factors released by activated T-cells play a key role in muscle satellite cell proliferation and migration, although the precise mechanisms of these interactions remain unclear. T-cells in older people display limited ability to activate satellite cell proliferation and migration which is likely to contribute to insufficient muscle repair and, consequently, muscle wasting and weakness. If the factors released by T-cells to activate satellite cells can be identified, it may be possible to develop therapeutic agents to enhance muscle regeneration and reduce the impact of muscle wasting during ageing and disease.     

细胞因子与癫痫

细胞因子 (ｃｙｔｏｋｉｎｅ)是神经 -内分泌 -免疫网络- 1,ＩＬ - 1)对脑组织内皮细胞的损伤并破坏血脑屏障[3] 。ＤｅＳｉｍｏｎｉ等[4 ] 的研究显示自发的惊厥发作伴经元和胶质细胞产生[8] 。脑内局部ＩＬ - 1β增高可加重脑炎引起的惊厥 ,惊厥患儿外周血单核细胞接受保护作用[2 0 ] 。Ｇｏｔｔｓｃｈａｌｋ等[2 1] 研究发现ＢＤＮＦ对神经系统的发育过程中对神经细胞有着重要的营养和ＢＤＮＦ)的影响具有双重性 ,更值得我们注意。细胞因子与癫痫@罗向阳$中山大学第二附属医院儿科!广东广州510120 @黄绍良$中山大学第二附属医院儿科!…     

骨骼肌通过力学刺激对骨重建的影响

骨骼与骨骼肌作为运动系统最重要的组织,两者之间存在密切的联系。骨肌单元的概念提出已久,运动产生的力学负荷将两者紧密地联系在一起。骨骼为骨骼肌施力提供力学支撑,而骨骼肌收缩带动机体的运动。在机体运动过程中,骨骼肌充当力学负荷与骨骼之间的中间媒介,并通过内分泌因子以及力学信号调节骨骼的代谢活动,与机体内持续不断的骨重建密切相关,并维持骨骼良好的结构和功能。主要综述近年来骨骼肌通过对骨骼施加力学刺激影响骨重建作用的研究进展,为预防和治疗骨代谢疾病提供新的思路。     

Prostanoids and MPO-halide system products as a link between innate and adaptive immunity

and The crosstalk between innate adaptive immunity is regulated by cytokines and complex interactions between cells of the immune system. A variety of endogenous agents are involved in the regulation of the cytokine network. Especially, eicosanoids and ROIs have a great impact on the regulation of cytokine production. Eicosanoids (prostanoids, leukotrienes and lipoxins) are produced mainly by inflammatory cells while their receptors are distributed on the cells of both arms of the immune system. Depending on the predominant prostanoid produced and the profile of prostanoid receptors expression on immune cells, eicosanoids can selectively regulate the production of Th1 and Th2 driven cytokines. Inflammatory cells (neutrophils, macrophages), are also a rich source of large amounts of ROIs. In this paper we have focused on the role of taurine chloramine (TauCl), the physiological product of neutrophil MPO-halide system, in the regulation of immune system. It is well documented that TauCl has pleiotropic effects on the inductive phase of the immune response. TauCl's immunoregulatory properties result from its ability to modulate the production of cytokines and eicosanoids. Finally, we conclude that eicosanoids and ROIs provide an important link between the afferent branches and the innate and adaptive immune response.     

废用性肌萎缩中ROS对蛋白质代谢的信号介导作用

废用性肌萎缩主要是由于蛋白质降解增强和蛋白质合成减弱导致的,对调节这一复杂过程的细胞信号通路的研究已取得了重要进展。越来越多的证据表明,活性氧自由基引起的氧化应激是细胞信号通路的重要调节因素,可导致长期废用时蛋白质降解增强和蛋白质合成减弱。本文主要讨论活性氧自由基（reactive oxygen species,ROS）对废用性肌萎缩蛋白质代谢的信号调节作用。