求一篇关于树突状细胞（dendritic cells,DC)的文献译文

求一篇关于树突状细胞（dendritic cells,DC)的文献译文
求一篇关于树突状细胞（dendritic cells,DC)的文献译文

求一篇关于树突状细胞（dendritic cells,DC)的文献译文
树突状细胞（Dendritic cells, DC）是机体功能最强的专职抗原递呈细胞(Antigen presenting cells, APC),它能高效地摄取、加工处理和递呈抗原,未成熟DC具有较强的迁移能力,成熟DC能有效激活初始型T细胞,处于启动、调控、并维持免疫应答的中心环节.
　　人树突状细胞起源于造血干细胞(hemopoieticstemcell).DC的来源有两条途径：①髓样干细胞在GM-CSF的刺激下分化为DC,称为髓样DC(myeloid dendritic cells,MDC),也称DCl,与单核细胞和粒细胞有共同的前体细胞；②来源于淋巴样子细胞,称为淋巴样DC(1ymophiod dendritic cells,LDC)或浆细胞样DC(plasmacytoid dendritic cells,piX；),即DC2,与T细胞和NK细胞有共同的前体细胞.树突状细胞(DC)尽管数量不足外周血单个核细胞的1%,但表面具有丰富的抗原递呈分子(MHC-Ⅰ和MHC-Ⅱ)、共刺激因子(CD80/B7-1、CD86/B7-2、CD40、CD40L等)和粘附因子(ICAM-1、ICAM-2、ICAM-3、LFA-1、LFA-3等),是功能强大的专职抗原递呈细胞(APC).DC自身具有免疫刺激能力,是目前发现的惟一能激活未致敏的初始型T细胞的APC.
　　人体内大部分DC处于非成熟状态,表达低水平的共刺激因子和粘附因子,体外激发同种混合淋巴细胞增殖反应的能力较低,但未成熟DC具有极强的抗原吞噬能力,在摄取抗原(包括体外加工)或受到某些因素刺激时即分化为成熟DC,而成熟的DC表达高水平的共刺激因子和粘附因子.DC在成熟的过程中,由接触抗原的外周组织迁移进入次级淋巴器官,与T细胞接触并激发免疫应答.
　　DC作为目前发现的功能最强的APC,能够诱导特异性的细胞毒性T淋巴细胞(cytotoxic T lymphocyte,CTL)生成.近年来研究表明,应用肿瘤相关抗原或抗原多肽体外冲击致敏DC,回输或免疫接种于载瘤宿主,可诱发特异性CTL的抗肿瘤免疫反应.
　　DC与肿瘤的发生、发展有着密切关系,大部分实体瘤内浸润的DC数量多则患者预后好.有效的抗肿瘤免疫反应的核心是产生以CD8+ T细胞为主体的细胞免疫应答,这也是DC作为免疫治疗手段的基础.
　　DC抗肿瘤的机制如下：①DC可以高表达MHC-Ⅰ类和MHC-Ⅱ类分子,MHC分子与其捕获加工的肿瘤抗原结合,形成肽-MHC分子复合物,并递呈给T细胞,从而启动MHC-I类限制性CTL反应和MHC-Ⅱ类限制性的CD4+ Thl反应.同时,DC还通过其高表达的共刺激分子(CD80/B7-1、CD86/B7-2、CD40等)提供T细胞活化所必须的第二信号,启动了免疫应答.②DC与T细胞结合可大量分泌IL-12、IL-18激活T细胞增殖,诱导CTL生成,主导Th1型免疫应答,利于肿瘤清除；激活穿孔素P颗粒酶B和FasL/Fas介导的途径增强NK细胞毒作用；③DC分泌趋化因子(Chemotactic Cytokines, CCK)专一趋化初始型T细胞促进T细胞聚集,增强了T细胞的激发.保持效应T细胞在肿瘤部位长期存在,可能通过释放某些抗血管生成物质(如IL-12、IFN-γ)及前血管生成因子而影响肿瘤血管的形成.上述CCK进一步以正反馈旁分泌的方式活化DC,上调IL-12及CD80、CD86的表达；同时DC 也直接向CD8+T细胞呈递抗原肽,在活化的CD4+ T细胞辅助下使CD8+ T细胞活化,CD4+ 和CD8+T细胞还可以进一步通过分泌细胞因子或直接杀伤,增强机体抗肿瘤免疫应答.
　　Dendritic cells (Dendritic cells, DC) is a function of the body most professional antigen presenting cells (Antigen presenting cells, APC), it can efficiently intake, processing and presenting antigen, immature DC has strong migration Ability to mature DC can effectively initial activation of T cells, at the start, control and maintain the immune response of the central link.
Origin of human dendritic cells in the hematopoietic stem cells (hemopoieticstemcell). DC is the source of two ways: ① myeloid stem cells in the GM-CSF to stimulate the differentiation of DC, known as medullary DC (myeloid dendritic cells, MDC), also known as DCl, with mononucleosis and tablets have a common cell Precursor cells; ② way from lymphatic cells, known as lymphoid DC (1ymophiod dendritic cells, LDC) or plasma cell-like DC (plasmacytoid dendritic cells, piX;), that is, DC2, and T cells and NK cells have a common ago Somatic cells. Dendritic cells (DC) Despite the insufficient number of peripheral blood mononuclear cells of one percent, but the surface is rich in antigen presenting molecules (MHC-Ⅰ and MHC-Ⅱ), a total of stimulating factor (CD80/B7-1, CD86 / B7-2, CD40, CD40L) and adhesion factor (ICAM-1, ICAM-2, ICAM-3, LFA-1, LFA-3), is a powerful professional antigen presenting cells (APC). DC has its own immune stimulation, and is now found not only sensitized to the initial activation of T cells in APC.
Most of the human body in a non-DC mature state, the low level of expression and adhesion factor stimulating factor, stimulated in vitro with the kind of mixed lymphocyte proliferation of low capacity, but is extremely immature DC antigen phagocytosis, in the uptake Antigen (including in vitro processing) or when stimulated by certain factors that differentiate into mature DC, DC and mature expression of a high level of total factor stimulating factor and adhesion. DC mature in the process of antigen from contact with the peripheral organizations move into the secondary lymphoid organs, and T-cell immune response and develop contacts.
DC found that the current function as the strongest APC, can induce specific cytotoxic T-lymphocytes (cytotoxic T lymphocyte, CTL) generated. In recent years research shows that the application of tumor-associated antigen, or antigen peptide in vitro impact sensitized DC, to lose or contained in the immunization of the host, can induce specific CTL anti-tumor immune response.
DC and tumor occurrence and development are closely related, most solid tumors, infiltrated a large number of DC, with a good prognosis. Effective anti-tumor immune response is to produce the core of CD8 + T cells as the main body of the cellular immune response, this is DC as the basis of immune therapy.
DC anti-tumor mechanisms are as follows: ① DC can be high expression of MHC-Ⅰ category and MHC-Ⅱ molecules, MHC molecules with the capture of the tumor antigen processing combination of a peptide - MHC molecules complex, and delivery presented to T cells, which initiates MHC - I kind of restrictive CTL response and MHC-Ⅱ restrictive type of CD4 + Thl response. At the same time, DC through its expression of costimulatory molecules (CD80/B7-1, CD86/B7-2, CD40, etc.) provided by the activation of T cells to be the second signal, activated the immune response. ② DC can be combined with the large number of T cells secreting IL-12, IL-18 activation of T-cell proliferation and induced CTL generation, Th1-type immune response, to tumor removal; activated P-piercing granzyme B and FasL / Fas-mediated way to enhance NK cytotoxicity; ③ DC secretion of chemokines (Chemotactic Cytokines, CCK) specific chemokine initial T cells to promote T-cell aggregation and enhanced the T cells stimulated. Maintain the effect of T cells in the tumor site exist for a long time, probably through the release of some anti-angiogenesis substances (such as IL-12, IFN-γ) and the former angiogenesis factor affecting the formation of tumor blood vessels. CCK further to the side of positive feedback form the secretion of activated DC, increased IL-12 and CD80, CD86 expression at the same time DC also directly to the CD8 + T cells presenting antigen, in the activation of CD4 + T cells assisted the CD8 + T cell activation , CD4 + and CD8 + T cells can be further through the secretion of cytokines or direct destruction, enhanced anti-tumor immune responses in the body.