共查询到19条相似文献,搜索用时 671 毫秒
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动脉粥样硬化,是冠心病的病理基础,被认为是一种慢性炎症性疾病,涉及如巨噬细胞和T淋巴细胞等许多炎性细胞。肥大细胞是一种重要的免疫细胞,其功能主要是在超敏反应方面的作用。有病理学研究表明:肥大细胞在动脉粥样硬化斑块周围表达增加,这表明肥大细胞可能与疾病的进展有关。最近的研究表明,肥大细胞在动脉粥样硬化中确实起着重要的作用。本文通过总结肥大细胞在动脉粥样硬化形成中的作用,为在疾病进程中,通过调节肥大细胞功能来改善动脉粥样硬化的这种治疗方式的可能性提供依据。 相似文献
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肝素(heparin)是由肥大细胞产生的内源性分子,是一种高度硫酸化的糖胺聚糖,随着肥大细胞脱颗粒与组胺等物质一起释放到细胞外基质中。因其主要与抗凝血酶III结合而增强其活性,间接发挥抗凝作用,故在临床上作为抗凝剂广泛使用。然而,肝素在体内的主要生物学功能仍不清楚。研究表明,肝素能够结合体内多种蛋白,影响许多生物信息的传递,在肥大细胞活性、炎症反应、细胞增殖分化及多种疾病中发挥重要作用。本文总结肝素研究的重要成果,对肝素的主要的生物学功能进行综述。 相似文献
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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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动脉粥样硬化与清道夫受体研究进展 总被引:1,自引:0,他引:1
动脉粥样硬化是最重大的疾病之一,是心脑血管病的主要病理基础,严重危害人类健康.近年来的研究表明,清道夫受体在胆固醇代谢中起着重要作用.清道夫受体是一类结构多样化的糖蛋白受体,具有广泛的配体谱和功能.已知清道夫受体与动脉粥样硬化、宿主防御、细胞粘附、细胞增殖以及细胞凋亡等均有不同程度的关系.文章就近几年来有关该受体的结构、分布、表达调控及其在动脉粥样硬化中作用作一综述,以探索防治途径. 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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Mast cell function and dysregulation is important in the development and progression of allergic and autoimmune disease. Identifying novel proteins involved in mast cell function and disease progression is the first step in the design of new therapeutic strategies. Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) are a family of proteins demonstrated to mediate the transport and fusion of secretory vesicles to the membrane in mast cells, leading to the subsequent release of the vesicle cargo through an exocytotic mechanism. The functional role[s] of specific SNARE family member complexes in mast cell degranulation has not been fully elucidated. Here, we review recent and historical data on the expression, formation and localization of various SNARE proteins and their complexes in murine and human mast cells. We summarize the functional data identifying the key SNARE family members that appear to participate in mast cell degranulation. Furthermore, we discuss the utilization of RNA interference (RNAi) methods to validate SNARE function and the use of siRNA as a therapeutic approach to the treatment of inflammatory disease. These studies provide an overview of the specific SNARE proteins and complexes that serve as novel targets for the development of new therapies to treat allergic and autoimmune disease. 相似文献
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Among the potential outcomes of an aberrantly functioning immune system are allergic disease and autoimmunity. Although it has been assumed that the underlying mechanisms mediating these conditions are completely different, recent evidence shows that mast cells provide a common link. Mast cells reside in most tissues, are particularly prevalent at sites of Ag entry, and act as sentinel cells of the immune system. They express many inflammatory mediators that affect both innate and adaptive cellular function. They contribute to pathologic allergic inflammation but also serve an important protective role in bacterial and parasite infections. Given the proinflammatory nature of autoimmune responses, it is not surprising that studies using murine models of autoimmunity clearly implicate mast cells in the initiation and/or progression of autoimmune disease. In this review, we discuss the defined and hypothesized mechanisms of mast cell influence on autoimmune diseases, including their surprising and newly discovered role as anti-inflammatory cells. 相似文献
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Human atherosclerosis has many characteristics of an inflammatory disorder. Recent data suggest that mast cells might be important in the pathogenesis of atherosclerotic disease. By secretion of pro-inflammatory cytokines, mast cells can assist in the recruitment of monocytes and lymphocytes into vascular tissue, thereby propagating the inflammatory response. Mast cell enzymes might activate pro-metalloproteinases, thereby destabilizing atheromatous plaques. Mast cells can facilitate foam cell formation by promoting cholesterol accumulation. However, mast cell tryptase could slow thrombus formation at sites of plaque rupture by interfering with coagulation. Therefore, mast cells can modulate coronary artery disease by both facilitatory and inhibitory pathways. 相似文献
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Mast cell degranulation can initiate an acute inflammatory response and contribute to the progression of chronic diseases. Alteration in the cellular programs that determine the requirement for mast cell degranulation would therefore have the potential to dramatically impact disease severity. Mast cells are exposed to increased levels of PGE2 during inflammation. We show that although PGE2 does not trigger the degranulation of dermal mast cells of young animals, in older mice, PGE2 is a potent mast cell stimulator. Intradermal administration of PGE2 leads to an EP3 receptor-dependent degranulation of mast cells, with the number of degranulated cells approaching levels observed in IgE- and Ag-treated controls. Taken together, these studies suggest that the ability of PGE2 to initiate mast cell degranulation changes in the aging animal. Therefore, elevated PGE2 levels might provide an important pathway by which mast cells are engaged to participate in inflammatory responses in the elderly patient. 相似文献
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IL-10 suppresses mast cell IgE receptor expression and signaling in vitro and in vivo 总被引:1,自引:0,他引:1
Kennedy Norton S Barnstein B Brenzovich J Bailey DP Kashyap M Speiran K Ford J Conrad D Watowich S Moralle MR Kepley CL Murray PJ Ryan JJ 《Journal of immunology (Baltimore, Md. : 1950)》2008,180(5):2848-2854
Mast cells are known for their roles in allergy, asthma, systemic anaphylaxis, and inflammatory disease. IL-10 can regulate inflammatory responses and may serve as a natural regulator of mast cell function. We examined the effects of IL-10 on in vitro-cultured mouse and human mast cells, and evaluated the effects of IL-10 on FcepsilonRI in vivo using mouse models. IgE receptor signaling events were also assessed in the presence or absence of IL-10. IL-10 inhibited mouse mast cell FcepsilonRI expression in vitro through a Stat3-dependent process. This down-regulation was consistent in mice tested in vivo, and also on cultured human mast cells. IL-10 diminished expression of the signaling molecules Syk, Fyn, Akt, and Stat5, which could explain its ability to inhibit IgE-mediated activation. Studies of passive systemic anaphylaxis in IL-10-transgenic mice showed that IL-10 overexpression reduced the IgE-mediated anaphylactic response. These data suggest an important regulatory role for IL-10 in dampening mast cell FcepsilonRI expression and function. IL-10 may hence serve as a mediator of mast cell homeostasis, preventing excessive activation and the development of chronic inflammation. 相似文献
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c-Fos as a regulator of degranulation and cytokine production in FcepsilonRI-activated mast cells 总被引:3,自引:0,他引:3
Lee YN Tuckerman J Nechushtan H Schutz G Razin E Angel P 《Journal of immunology (Baltimore, Md. : 1950)》2004,173(4):2571-2577
The AP-1 complex is composed of c-Jun and c-Fos and is a key component in the regulation of proinflammatory genes. Mast cells play a significant role in the initiation of many inflammatory responses, such as allergy and allergy-associated diseases. In the present work, we characterized the role of c-Fos in mast cell function by investigating IL-3-dependent cell proliferation, degranulation capability, and cytokine expression in c-Fos-deficient mice. In c-Fos-deficient mast cells, we found that FcepsilonRI-mediated degranulation was significantly inhibited, which correlates with the reduced expression of SWAP-70, VAMP-7, and Synaptotagmin I genes, which are involved directly in the degranulation process. These findings show that c-Fos plays an important role in FcepsilonRI-mediated regulation of mast cell function. 相似文献
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张秩源唐惠芳 《现代生物医学进展》2012,12(22):4396-4400
动脉粥样硬化是一种慢性炎症过程,炎症反应在动脉粥样斑块的形成、发展、稳定性丧失和斑块破裂过程中都起着非常重要的作用,贯穿于动脉粥样硬化的各个环节。从早期的脂质条纹到进一步的动脉粥样病变及血栓性并发症都能见到炎症细胞的浸润,其中又以激活的巨噬细胞尤为重要。新蝶呤是巨噬细胞激活后的代谢产物,它不仅是巨噬细胞激活的炎症标志物,还参与多种调节氧化平衡的生化途径,增加氧化应激水平,促进动脉粥样硬化的进展,是斑块不稳定性及不良性心血管事件的独立预测因子。在临床上,降低血清新蝶呤水平可以降低冠心病患者发生危险事件的风险。因此,新蝶呤对冠心病的诊断和治疗都有重要意义。本文将对新蝶呤在冠心病中的角色做一综述。 相似文献
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慢性炎症与动脉粥样硬化关系的研究进展 总被引:1,自引:0,他引:1
动脉粥样硬化(atherosclerosis,AS)的发病机制非常复杂,对其研究经历了一个半世纪,直到1999年Ross提出"动脉粥样硬化是一种炎症性疾病",各种炎症细胞和炎症因子参与动脉粥样硬化的发生和发展过程。已有众多的基础和临床研究都证实炎症在AS中的重要作用,但仍需要对AS发生发展的深入研究,使我们更准确认识和有效的防治AS。本文就近年来慢性炎症与动脉粥样硬化关系的研究进展作一综述。 相似文献