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《微生物学免疫学进展》2017,(1)
自从Paul Ehrlich于1878年首次发现肥大细胞以来,肥大细胞作为过敏反应中非常重要的效应细胞之一被广泛研究。直到近20年,人们才逐渐认识到肥大细胞参与多种病理、生理过程,尤其是在机体抗感染、免疫与免疫病理损伤中也发挥着重要作用。随着人们对肥大细胞在细菌和寄生虫的抗感染、免疫中作用的理解不断深入,肥大细胞在病毒感染及病毒引起的相关疾病中的作用逐渐成为备受关注的研究热点,现就肥大细胞在不同病毒感染中的作用作一综述。 相似文献
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肥大细胞(mast cells)起源于骨髓造血干细胞,定植到机体各个外周组织后继续发育成熟,在过敏性反应和预防微生物感染等方面发挥重要作用。近来研究发现,肥胖患者的脂肪组织含有大量肥大细胞,引发人们对脂肪组织中肥大细胞作用的关注。肥大细胞可释放出多种生物活性介质,作用于脂肪组织,影响脂肪组织中细胞外基质的重塑和各种炎性细胞的活动。更多研究还表明肥大细胞可能参与到肥胖、糖尿病等代谢性疾病的发病机理,影响疾病的进展。本文总结近年来对脂肪组织中肥大细胞研究的一系列成果,对肥大细胞在脂肪组织中的生物学作用进行综述。 相似文献
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巨噬细胞是机体免疫系统的重要一员,具有趋化、吞噬、免疫及分泌等功能。在动脉粥样硬化(atherosclerosis,AS)形成过程中,巨噬细胞受低密度脂蛋白氧化修饰过程中的炎性因子趋化,大量吞噬氧化低密度脂蛋白,变为"泡沫细胞",进而导致动脉粥样硬化病变,并通过免疫及分泌功能生成肿瘤坏死因子α等物质加速病变的进展,其功能变化与动脉粥样硬化形成和发展息息相关。ADRP作为PAT家族蛋白中的一员,因在脂滴形成中的重要作用而受到广泛关注。ADRP是动脉粥样硬化过程中的一个关键分子,不仅在病变中起着提高炎症反应与调节脂质代谢的双重作用,而且通过限制泡沫细胞的形成,而影响了动脉粥样硬化的走向。 相似文献
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近年来研究资料表明,肥大细胞参与获得性免疫应答,提供对CD4^+和CD8^+T细胞的协同刺激,并可释放对B细胞的殖和分化信号。这些功能在细菌性感染和线虫感染中均有其表现,并与这些感染的免疫防护有关,肥大细胞可通过启动或控制对抗细菌或寄生虫感染的T和B细胞表型来完成其对特异性免疫调节功能。对于肥大细胞功能的深入了解将有助于许多生理及免疫病理机制的阐明。 相似文献
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微粒是血管内皮细胞、组织细胞或血细胞激活或凋亡时形成的亚微型囊泡。动脉粥样硬化时血浆及粥样斑块中富含多种细胞来源的微粒,不仅促进斑块的发生发展并且在动脉粥样硬化凝血异常中起重要作用,可增进血管内皮细胞和白细胞间的相互作用,使单核细胞粘附于内皮细胞,从而迁移到斑块内,吞噬清除内膜下沉积的脂质。巨噬细胞吞噬脂质后凋亡形成大量微粒,抑制内皮细胞合成释放一氧化氮,加重内皮细胞损伤,促进斑块扩大。微粒表面富含的磷脂酰丝氨酸和组织因子是微粒促凝活性的主要来源,病灶处及循环中存在的大量微粒促进了动脉粥样硬化时凝血异常的发生。本文将就微粒在动脉粥样硬化形成及凝血异常中的作用做一综述。 相似文献
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肥大细胞是人体主要免疫细胞之一,因其作为导致过敏反应发生的最直接效应细胞而著称.肥大细胞最主要的结构特征为其胞内含有大量嗜碱性颗粒,该颗粒内又富含种类众多的生物活性物质,包括组胺、血管内皮生长因子(vascular endothelial growth factor,VEGF)、成纤维细胞生长因子(fibroblast... 相似文献
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应用组织化学、免疫组织化学、电子显微镜及形态测量等方法对二乙基亚硝胺(DEN)诱发大鼠肝肿瘤过程中肥大细胞(MC)对肝细胞生化代谢、细胞核及核仁组成区(NOR)的影响等进行了研究。结果显示肝细胞葡萄糖6磷酸酶(G-6-Pase)和α-抗胰蛋白酶(α-AT)在MC最多与最少组之间的分布无明显差异,而嗜银蛋白颗粒(AgNOR)计数和纤维中心数密度及核仁面积之比则自第十四周起显示出分布的个体差异,它们在MC最多组明显低于MC最少组、本文并对该种差异的意义进行了简要讨论。 相似文献
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Puxeddu I Piliponsky AM Bachelet I Levi-Schaffer F 《The international journal of biochemistry & cell biology》2003,35(12):1601-1607
Mast cells (MC) are highly granulated tissue dwelling cells, widely distributed throughout the body in connective tissues and on mucosal surfaces. They are derived from bone marrow progenitors that migrate into the blood and subsequently into the tissues, where they undergo final maturation. Mast cell proliferation, differentiation, survival and activation are regulated by stem cell factor, the ligand for the c-kit tyrosine kinase receptor, expressed on the mast cell surface. They release a large number of pro-inflammatory and immunoregulatory mediators after activation induced by either immunoglobulin E-dependent or immunoglobulin E-independent mechanisms. Mast cells have been most widely studied in the context of allergic reactions and parasite infections, but there is now compelling evidences that they are important players in innate and acquired immunity, wound healing, fibrosis, tumors and autoimmune diseases. This review will discuss current advances in these fields.Cell facts
- • Mast cells are high affinity IgE receptor bearing tissue dwelling cells containing prominent cytoplasmic granules and key cells in allergy.
- • Mast cell proliferation, differentiation, survival and activation are regulated by stem cell factor.
- • Mast cells and their mediators participate in innate and acquired immunity, wound healing, tissue remodeling, angiogenesis and autoimmune diseases.
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Accumulation of mast cells (MCs) in tumours was described by Ehrlich in his doctoral thesis. Since this early account, ample evidence has been provided highlighting participation of MCs to the inflammatory reaction that occurs in many clinical and experimental tumour settings. MCs are bone marrow-derived tissue-homing leukocytes that are endowed with a panoply of releasable mediators and surface receptors. These cells actively take part to innate and acquired immune reactions as well as to a series of fundamental functions such as angiogenesis, tissue repair, and tissue remodelling. The involvement of MCs in tumour development is debated. Although some evidence suggests that MCs can promote tumourigenesis and tumour progression, there are some clinical sets as well as experimental tumour models in which MCs seem to have functions that favour the host. One of the major issues linking MCs to cancer is the ability of these cells to release potent pro-angiogenic factors. This review will focus on the most recent acquisitions about this intriguing field of research. This article is part of a Special Issue entitled: Mast cells in inflammation. 相似文献
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Mast cells are important mediators of normal angiogenesis, and participate in normal would healing, i.e. processes involved in pancreatic islet engraftment. The aim of the study was to evaluate if mast cells are present in islet grafts. For this purpose, male normoglycaemic Wistar-Furth rats were either untreated or syngeneically implanted with 250 islets under the renal capsule. The animals were killed 1 month later, and the kidneys and endogenous pancreas were removed, fixed and embedded in paraffin. The distribution of mast cells was studied in Alcian Blue stained sections. Mast cells were rarely encountered in endogenous islets, but were frequent in the renal capsule adjacent to islet grafts. Mast cells interspersed between graft endocrine cells were as rare as in the endogenous pancreas. We conclude that mast cells may contribute to the engraftment after islet transplantation. 相似文献
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Martha Balázs György Illyés Gizella Vadász 《Virchows Archiv. B, Cell pathology including molecular pathology》1989,57(1):353-360
The changes in the number and ultrastruture of mast cells were studied in 37 colonoscopical biopsies from patients with ulcerative
colitis. Changes in the active stage of the disease and during remission were compared. Cell counts were performed on semithin
sections stained with Giemsa after osmium tetroxide fixation. This method overcome the uncertain staining found after formalin
fixation. Accumulation of mast cells accompanied by intense degranulation was found to be significant in the active stage
of the disease. Two forms of degranulation were observed: discharge of the individual granules and protrusion and detachment
of the cytoplasmic processes containing granules. The latter was a sign of rapid degranulation, as described earlier in animal
experiments. Mast cells were closely associated with capillary blood vessels, Schwann cells, neural fibres, myofibroblasts
and collagenous fibres, and were also present between epithelial cells. It is assumed that close topographic contact may also
imply a functional correlation. 相似文献
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The link between atherosclerosis and regions of disturbed flow and low wall shear stress is now firmly established, but the causal mechanisms underlying the link are not yet understood. It is now recognised that the endothelium is not simply a passive barrier between the blood and the vessel wall, but plays an active role in maintaining vascular homeostasis and participates in the onset of atherosclerosis. Calcium signalling is one of the principal intracellular signalling mechanisms by which endothelial cells (EC) respond to external stimuli, such as fluid shear stress and ligand binding. Previous studies have separately modelled mass transport of chemical species in the bloodstream and calcium dynamics in EC via the inositol trisphosphate (IP(3)) signalling pathway. We review existing models of these two phenomena, before going on to integrate the two components to provide an inclusive new model for the calcium response of the endothelium in an arbitrary vessel geometry. This enables the combined effects of fluid flow and biochemical stimulation on EC to be investigated and is the first time spatially varying, physiological fluid flow-related environmental factors have been combined with intracellular signalling in a mathematical model. Model results show that low endothelial calcium levels in the area of disturbed flow at an arterial widening may be one contributing factor to the onset of vascular disease. 相似文献
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Keiko Kan-o Yuko Matsunaga Satoru Fukuyama Atsushi Moriwaki Hiroko Hirai-Kitajima Takehiko Yokomizo Kosuke Aritake Yoshihiro Urade Yoichi Nakanishi Hiromasa Inoue Koichiro Matsumoto 《Respiratory research》2013,14(1):28
Background
Clinical studies showed the contribution of viral infection to the development of asthma. Although mast cells have multiple roles in the pathogenesis of allergic asthma, their role of in the virus-associated pathogenesis of asthma remains unknown. Most respiratory viruses generate double-stranded (ds) RNA during their replication. dsRNA provokes innate immune responses. We recently showed that an administration of polyinocinic polycytidilic acid (poly IC), a mimetic of viral dsRNA, during allergen sensitization augments airway eosinophilia and hyperresponsiveness in mice via enhanced production of IL-13.Methods
The effect of poly IC on allergen-induced airway eosinophilia was investigated for mast cell-conserved Kit+/+ mice and -deficient KitW/KitW-v mice. The outcome of mast cell reconstitution was further investigated.Results
Airway eosinophilia and IL-13 production were augmented by poly IC in Kit+/+ mice but not in KitW/KitW-v mice. When KitW/KitW-v mice were reconstituted with bone marrow-derived mast cells (BMMCs), the augmentation was restored. The augmentation was not induced in the mice systemically deficient for TIR domain-containing adaptor-inducing IFN-β (TRIF) or interferon regulatory factor (IRF)-3, both mediate dsRNA-triggered innate immune responses. The augmentation was, however, restored in KitW/KitW-v mice reconstituted with TRIF-deficient or IRF-3-deficient BMMCs. Although leukotriene B4 and prostaglandin D2 are major lipid mediators released from activated mast cells, no their contribution was shown to the dsRNA-induced augmentation of airway eosinophilia.Conclusions
We conclude that mast cells contribute to dsRNA-induced augmentation of allergic airway inflammation without requiring direct activation of mast cells with dsRNA or involvement of leukotriene B4 or prostaglandin D2. 相似文献18.
Mast cells are located in close proximity to neurons in the peripheral and central nervous systems, suggesting a functional role in normal and aberrant neurodegenerative states. They also possess many of the features of neurons, in terms of monoaminergic systems, responsiveness to neurotrophins and neuropeptides and the ability to synthesise and release bioactive neurotrophic factors. Mast cells are able to secrete an array of potent mediators which may orchestrate neuroinflammation and affect the integrity of the blood-brain barrier. The cross-talk between mast cells, lymphocytes, neurons and glia constitutes a neuroimmune axis which is implicated in a range of neurodegenerative diseases with an inflammatory and/or autoimmune component, such as multiple sclerosis and Alzheimer's disease. Mast cells appear to make an important contribution to developing, mature and degenerating nervous systems and this should now be recognised when assessing the neurotoxic potential of xenobiotics.Abbreviations AChE
acetylcholinesterase
- ALS
amyotrophic lateral sclerosis
- APP
amyloid precursor protein
- BBB
blood-brain barrier
- BDNF
brain-derived neurotrophic factor
- CGRF
calcitonin gene-related peptide
- CNS
central nervous system
- CNTF
ciliary neurotrophic factor
- CSF
cerebrospinal fluid
- C48/80
compound 48/80
- CTMC
connective tissue mast cells
- EAA
excitatory amino acids
- EAE
experimental allergic encephalomyelitis
- ECMA
ethylcholine mustard aziridinium ion
- FACS
fluorescent activated cell sorter
- 5HT
5-hydroxytryptamine (serotonin)
- HMT
histamine-N-methyltransferase
- HPMC
human placental mast cells
- HRNGF
human recombinant nerve growth factor
- IgE
immunoglobulin E
- MMC
methyl mercuric chloride
- MAOI
monoamine oxidase inhibitors
- MDMA
methylenedioxymetamphetamine
- MS
multiple sclerosis
- NGF
nerve growth factor
- NT3
neurotrophin 3
- PNS
peripheral nervous system
- RBMC
rat brain mast cells
- ROS
reactive oxygen species
- RPMC
rat peritoneal mast cells
- SLE
systemic lupus erythematosus
- SP
substance P
- TCA
trichloroacetic acid
- THA
tetrahydroacridine
- TCA
tricyclic antidepressants
Special issue dedicated to Dr. Robert Balázs. 相似文献
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Jie ZhangGuo-Ping Shi 《生物化学与生物物理学报:疾病的分子基础》2012,1822(1):14-20
Mast cells are critical effectors in the development of allergic diseases and in many immunoglobulin E-mediated immune responses. These cells exert their physiological and pathological activities by releasing granules containing histamine, cytokines, chemokines, and proteases, including mast cell-specific chymase and tryptase. Like macrophages and T lymphocytes, mast cells are inflammatory cells, and they participate in the pathogenesis of inflammatory diseases such as cardiovascular complications and metabolic disorders. Recent observations suggested that mast cells are involved in insulin resistance and type 2 diabetes. Data from animal models proved the direct participation of mast cells in diet-induced obesity and diabetes. Although the mechanisms by which mast cells participate in these metabolic diseases are not fully understood, established mast cell pathobiology in cardiovascular diseases and effective mast cell inhibitor medications used in pre-formed obesity and diabetes in experimental models offer hope to patients with these common chronic inflammatory diseases. This article is part of a Special Issue entitled: Mast cells in inflammation. 相似文献