嗜酸性粒细胞在蠕虫感染免疫中的作用

嗜酸性粒细胞增多是蠕虫感染的重要特征。蠕虫造成的宿主上皮损伤能诱导2型免疫细胞的激活和分化。其中,嗜酸性粒细胞在细胞因子、趋化因子以及黏附分子的作用下发育成熟并募集到蠕虫感染部位,通过分泌一系列颗粒蛋白与免疫调节因子发挥免疫效应。本文就嗜酸性粒细胞和蠕虫之间关系的最新进展进行综述,探讨嗜酸性粒细胞对宿主的保护性免疫与病理损伤的两面性,及其对宿主机体的免疫调节作用。     

嗜酸性粒细胞与组织免疫损伤

嗜酸性料细胞（ＥＯ）的特殊颗粒中含有主要碱性蛋白（ＭＢＰ），嗜酸性粒细胞离子蛋白（ＥＣＰ），嗜酸性粒细胞衍生的神经毒素（ＥＤＮ），嗜酸性粒细胞过氧化物酶（ＥＰＯ）等强碱性蛋白，脱颗粒引起上述物质的释放。ＥＯ通过强碱性蛋白和活性氧引起组织细胞损伤，ＥＯ还可以产生ＰＡＦ，ＬＴＣ４，ＬＴＤ４等炎性介质而引起炎症反应，因而多种疾病可能与ＥＯ相关。     

低密度嗜酸性粒细胞

本文介绍了低密度嗜酸性粒细胞（ＨＥｏ）与疾病的关系及ＨＥｏ产生的机制。对ＨＥｏ与正常密度嗜酸性粒细胞，在形态学，细胞成分，功能代谢，膜受体及表面蛋白等方面的差异进行了比较。认为ＨＥｏ在一定程度上反映了嗜酸性粒细胞的活化。     

嗜酸性粒细胞阳离子蛋白在支气管哮喘中的研究

嗜酸性粒细胞阳离子蛋白(ECP)是活化嗜酸性细胞释放的强碱性蛋白中的重要组分,是嗜酸性粒细胞活化的重要标志,本文概述了ECP的来源,生物学作用以及与感染的关系,着重综述了ECP与支气管哮喘之间的关系。     

中性粒细胞在肿瘤免疫中的研究进展

肿瘤微环境中的中性粒细胞分为具有抗肿瘤效应的N1 型和促肿瘤效应的N2 型。N1 型中性粒细胞抑制、杀伤肿瘤细胞发挥抗肿瘤作用;N2 型中性粒细胞可以通过释放弹性蛋白酶、基质金属蛋白酶、细胞因子和趋化因子等方式,促进肿瘤的发生、生长和转移及肿瘤血管生成。本文就中性粒细胞的生物学特性与肿瘤发生发展等方面,综述中性粒细胞在肿瘤免疫中的研究进展。     

NO—cGMP途径在嗜酸性粒细胞功能中作用的研究进展

一氧化氮是具有高度反应性的自由基 ,在体内广泛存在 ,是一种重要的细胞内信号转导分子 ,在细胞多种功能中起作用。NO主要通过提高环一磷酸鸟苷水平来实现其生物学功能。NO cGMP途径在嗜酸性粒细胞的功能中起重要作用 ,嗜酸性粒细胞在哮喘过程中能产生大量NO。两者之间存在密切联系。本文主要介绍NO cGMP信号转导通路、该通路在嗜酸性粒细胞趋化 ,凋亡等功能中作用以及NO释放在哮喘中意义的研究进展。     

嗜酸性粒细胞募集在支气管哮喘发病中的作用

支气管哮喘是一种气道慢性炎症性疾病,伴有嗜酸性粒细胞增多、杯状细胞肥大、黏液分泌增多、可逆性的气道阻塞及对吸入变应原和非特异性刺激的高反应性等特点,其中嗜酸性粒细胞募集和随后的激活在支气管哮喘发病中起着十分重要的作用。本文就嗜酸性粒细胞募集在支气管哮喘发病机制中的研究进展作一综述,为支气管哮喘的治疗提供一线新的曙光。     

嗜酸性粒细胞活化趋化因子与支气管哮喘的研究进展

嗜酸性粒细胞活化趋化因子(Eotaxin)是CC趋化因子家族成员之一,由结构性细胞和渗出性炎症细胞产生,是嗜酸性粒细胞、嗜碱性粒细胞和Th2型细胞因子的化学激活趋化剂,通过其受体(CCR3)选择性地诱导嗜酸性粒细胞在肺内黏附、募集和脱颗粒。     

哮喘患者痰嗜酸性粒细胞凋亡与IL-5及sIL-2R相关性的研究

目的：探讨哮喘患者痰液嗜酸性粒细胞凋亡(EOS)与IL-5和sIL-2R的关系。方法：选择哮喘患者(哮喘组)急性发作期和缓解期30例，20名健康人(正常组)作对照。分别采用ELISA法测定患者痰液白细胞介素5(IL-5)和可溶性白介素2受体(sIL-2R)，应用流式细胞仪检测痰液EOS凋亡。结果：哮喘患者急性发作期和缓解期痰液中IL-5和sIL-2R明显升高，EOS凋亡率增高，而正常组未发现EOS凋亡。急性发作期哮喘患者EOS凋亡率与IL-5呈明显的负相关，r为～0.78。结论：哮喘患者气道局部有EOS凋亡现象，并受到IL-5相互作用的调节。sIL-2R与EOS凋亡率无明显的相关性。     

气道嗜酸性粒细胞增高与COPD加重

有证据表明部分COPD加重期气道嗜酸性粒细胞增高 ,其原因可能与病毒感染有关 ;了解COPD加重期气道嗜酸性粒细胞增高的发病机制 ,认识伴有嗜酸性粒细胞增高的气道炎症对临床治疗中是否选择糖皮质激素有一定价值 ,本文就这方面进展作一综述     

调节性T细胞参与肿瘤免疫的研究进展

调节性T细胞（Treg）对于介导免疫稳态、建立和维持自身耐受有重要作用.其对免疫反应具有抑制效应,保护机体免于发生自身免疫性疾病,并且可以抑制抗肿瘤免疫反应.近来研究发现,多种恶性肿瘤的患者外周血及肿瘤微环境中（Treg）增加,并且与预后具有相关性;去除Treg或者封闭其抑制功能可以增强抗肿瘤免疫反应.越来越多的证据表明Treg在肿瘤的进展过程和抑制肿瘤特异性免疫中扮演重要的角色.深入研究Treg的特点、功能和参与肿瘤免疫调节作用的机制将给肿瘤的预防和治疗提供新的思路和有效手段.     

肿瘤炎性微环境与树突状细胞研究进展

肿瘤免疫是近年来的研究热点,已知肿瘤微环境尤其是炎性微环境在促进肿瘤发生、发展过程中起重要作用。肿瘤浸润的树突状细胞（DC）多存在表型未成熟化、分布异常及功能障碍等现象,这可能是肿瘤诱导机体免疫耐受的重要机制之一。肿瘤炎性微环境可通过多种途径调节DC的分化和成熟,相关信号通路和分子机制正逐步得到阐明,此将为DC疫苗的研制和肿瘤免疫治疗提供新的希望。     

Leptin-mediated cytokine release and migration of eosinophils: implications for immunopathophysiology of allergic inflammation

Leptin is a pleiotropic adipocyte-derived cytokine used in hypothalamic regulation of body weight and modulation of immune response by stimulating T cells, macrophages and neutrophils. Leptin has been shown to be an eosinophil survival factor. We examined the immunopathological mechanisms for the activation of human eosinophils from healthy volunteers by leptin in allergic inflammation. Adhesion molecules, cytokines and cell migration were assessed by flow cytometry, ELISA and Boyden chamber assay, respectively. Intracellular signaling molecules were investigated by membrane array and Western blot. Leptin could up-regulate cell surface expression of adhesion molecule ICAM-1 and CD18 but suppress ICAM-3 and L-selectin on eosinophils. Leptin could also stimulate the chemokinesis of eosinophils, and induce the release of inflammatory cytokines IL-1beta and IL-6, and chemokines IL-8, growth-related oncogene-alpha and MCP-1. We found that leptin-mediated induction of adhesion molecules, release of cytokines and chemokines, and chemokinesis were differentially regulated by the activation of ERK, p38 MAPK and NF-kappaB. In view of the above results and elevated production of leptin in patients with allergic diseases such as atopic asthma and atopic dermatitis, leptin could play crucial immunopathophysiological roles in allergic inflammation by activation of eosinophils via differential intracellular signaling cascades.     

Role of monocytes and eosinophils in human respiratory syncytial virus infection in vitro

RSV infection in airway epithelial cells (EC) results in production of the chemokines RANTES and MIP1alpha and the leukocyte differentiation factor GM-CSF. The chemokines attract monocytes and eosinophils to the site of infection, where GM-CSF may influence their function and differentiation. In turn, these inflammatory cells may limit the progression of RSV infection, as well as initiate immune responses. In the present study, the effect of monocytes and eosinophils on viral replication and infection-dependent release of EC-derived cytokines was investigated. The modulation of immune cell costimulatory molecules, CD80, CD86, CD40, and HLA-DR, and the release of the CD4(+) T cell chemoattractant IL-16 were also investigated. Employing immunofluorescence techniques, monocytes and eosinophils in cocultures with infected EC were found to inhibit the spread of RSV to uninfected cells. Monocytes also had a significant effect on replication of RSV. Monocytes phagocytized the virus, while eosinophils inhibited reinfection mainly by extracellular means. The release of G-CSF and GM-CSF in the infected cultures was not significantly affected by either monocytes or eosinophils, while RANTES release was significantly decreased. The expression of CD40, CD80, CD86, and HLA-DR on monocytes, but not on eosinophils, increased in an RSV-dose-dependent manner. IL-16 release was not induced in RSV-infected EC, but was significantly increased in coculture with monocytes. These results suggest that both monocytes and eosinophils attracted to the site of RSV infection play an important role in confining infection, while RSV-exposed monocytes may be involved in promoting/polarizing immune responses to RSV.     

Eotaxin-1-regulated eosinophils have a critical role in innate immunity against experimental Brugia malayi infection

Using two models of filarial infection in which Brugia malayi microfilariae (Mf) are contained in distinct anatomical compartments, in blood or tissue sites, we have demonstrated a critical role for eotaxin-1 in parasite clearance. In the first model, implantation of adult B. malayi into the peritoneal cavity of eotaxin-1(-/-) mice resulted in increased Mf survival associated with a dramatic reduction in peritoneal cavity eosinophilic infiltration. In the second model Mf were injected intravenously into eotaxin-1(-/-) mice; Mf clearance from the blood was more rapid than in wild-type mice and was associated with a pronounced blood eosinophilia, resulting from the inability of eosinophils to migrate to tissue sites in the absence of eotaxin-1. (Eotaxin-1 + IL-5)(-/-) mice had extended Mf survival in the blood and significantly reduced blood eosinophil levels. Interestingly, rapid clearance of a secondary Mf infection following immunization was unaltered in either eotaxin-1(-/-) mice or (eotaxin-1 + IL-5)(-/-) mice. Eosinophil peroxidase levels were high during primary, but not secondary infection, suggesting that eosinophil degranulation is important during primary Mf clearance. Thus, our data show that the presence of eosinophils is critical for innate clearance of B. malayi Mf infection, whereas rapid clearance of secondary infections is independent of both eotaxin-1 and IL-5.     

T细胞亚群在肿瘤微环境中的作用

根据T细胞亚群的不同,T细胞在肿瘤免疫中起着不同的重要作用.其能够对肿瘤组织产生不同的影响,进而引起肿瘤免疫的复杂性、双向性.因而深入了解肿瘤微环境中各T细胞亚群的功能及相互作用,能够对肿瘤的治疗提供重要依据.因此,对T细胞不同亚群在肿瘤中的作用进行研究具有重要意义.     

Interleukin (IL)-24 transforms the tumor microenvironment and induces anticancer immunity in a murine model of colon cancer

Interleukin-24 (IL-24) is a novel tumor suppressor and can mediate the induction of Th1-type cytokines from peripheral blood mononuclear cells. The individual properties of IL-24 have been previously examined; however, its in vivo immunological consequences and antitumor properties have not been previously evaluated with respect to colon cancer, the most commonly diagnosed cancer in China. Thus, we evaluated whether IL-24 could inhibit the progression of colon cancer in murine models with intact immune competence and explored the mechanisms underlying the immunological effects of IL-24 on colon cancer progression in vivo. In these murine models, we found that IL-24 promoted CD4⁺ T cells and CD8⁺ T cells to secrete interferon gamma and enhanced the cytotoxicity of CD8⁺ T cells in vivo. More importantly, we demonstrated that IL-24 transformed the tumor microenvironment and enhanced antitumor effects in favor of tumor eradication. Additionally, IL-24 expression correlated inversely with the clinical stage of human colorectal cancer. Thus, our study establishes a role of IL-24 in promoting antitumor immune responses and supports the development of a novel cytokine immunotherapy against colon cancer.     

Toll样受体与肿瘤

Toll样受体的发现是近二十年整个医学领域的一项重大发现.Toll样受体作为先天免疫的重要组成部分,是一种模式识别受体.它通过识别病原相关分子模式在机体天然免疫应答中发挥重要作用.Toll样受体不仅仅表达在免疫细胞,同样也表达在肿瘤细胞,影响着肿瘤的发生、发展.Toll样受体激活可发挥抗肿瘤的作用,但也可促进肿瘤的进展.人们对这截然相反的结果的发生机制还了解甚少.Toll样受体还能识别损伤相关分子模式形成慢性炎症微环境影响肿瘤的发生、发展、治疗.本文对Toll样受体与肿瘤之间的关系及相应研究最新进展进行综述.     

肿瘤相关性成纤维细胞与肿瘤关系的初探

肿瘤相关性成纤维细胞(tumor associated fibroblast,TAF)是肿瘤间质中的重要成员之一,随着肿瘤微环境的深入研究,其与肿瘤的相互关系已日益受到重视.TAF可以通过分泌多种细胞因子参与肿瘤的发生、发展、侵袭、转移及血管生成等过程,针对TAF的肿瘤靶向治疗也已悄然兴起.该文就TAF与肿瘤发生发展的关系加以综述.     

外泌体在结直肠癌中的研究进展

近年来,由于对外泌体的不断认识和了解,研究外泌体已成为当下的热点,外泌体是细胞分泌的一种纳米级囊泡结构,可来源于机体正常细胞及肿瘤细胞,在血液、唾液、尿液、母乳等多种体液中均有分布,其参与许多生物学和病理学过程,主要是由于它们在细胞间通讯作用,源自结直肠癌（CRC）细胞的外泌体与肿瘤发生、进展、转移、预后等相关。本文就外泌体在结直肠癌中的研究进展进行综述。