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首页> 外文学位 >Dendritic cell development and distribution in Type I diabetes: Overcoming genetic defects and establishing tolerance via pharmacotherapeutic manipulation of dendritic cell population in vivo.
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Dendritic cell development and distribution in Type I diabetes: Overcoming genetic defects and establishing tolerance via pharmacotherapeutic manipulation of dendritic cell population in vivo.

机译：I型糖尿病中树突状细胞的发育和分布：通过体内树突状细胞群体的药物治疗操作，克服遗传缺陷并建立耐受性。

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摘要

As the most potent antigen-presenting cell of the immune system, the dendritic cell has the unique capacity to both initiate and regulate antigen-specific immune responses. In the normally functioning immune system, the combination of costimulatory molecules and cytokines presented with MHC-peptide complexes on dendritic cells determine the penultimate function of naive antigen-specific T cells. Thus, scientist's have great interest in the function of dendritic cells in autoimmune disease, where self-reactive T cells are activated in the periphery and regulation of this response is deficient. This study demonstrates abnormalities of dendritic cell subsets within secondary lymphoid tissues of the autoimmune-prone NOD mouse and demonstrates a genetic basis for abnormalities of these cells in vivo. Studies where hematopoeitic progenitors were cultured with GM-CSF and IL-4 showed that NOD stem cells have a limited capacity to differentiate to fully mature dendritic cells. Analysis of several congenic mouse strains have identified this as a genetically controlled phenomenon, and further indicates potential in vivo differentiation and functional abnormalities that may lead to a dysfunctional immune system. Finally, activation of a lymphoid cell population known to interact with dendritic cells, the NK-T cell, is capable of limiting pancreatic beta cell destruction, apparently by initiating the emigration of dendritic cells from the pancreas to the draining lymph node, thus decreasing islet inflammation. Together, these findings establish a crucial role for abnormal dendritic cell development in the initiation and resolution of beta cell destruction in Type I diabetes.
机译：作为免疫系统中最有效的抗原呈递细胞，树突状细胞具有独特的能力来启动和调节抗原特异性免疫反应。在正常运转的免疫系统中，在树突状细胞上与MHC-肽复合物一起呈现的共刺激分子和细胞因子的结合决定了幼稚抗原特异性T细胞的倒数第二个功能。因此，科学家对树突状细胞在自身免疫性疾病中的功能非常感兴趣，在树突状细胞中，自身反应性T细胞在外周被激活，并且这种反应的调节不足。这项研究证明了自身免疫易发性NOD小鼠继发淋巴组织内树突状细胞亚群的异常，并证明了这些细胞异常的体内遗传基础。用GM-CSF和IL-4培养造血祖细胞的研究表明，NOD干细胞分化为完全成熟的树突状细胞的能力有限。对几种同基因小鼠品系的分析已将其鉴定为遗传控制现象，并进一步表明了潜在的[italic>体内分化和功能异常，可能导致免疫系统功能异常。最后，激活与树突状细胞（NK-T细胞）相互作用的淋巴样细胞群能够限制胰腺β细胞的破坏，显然是通过启动树突状细胞从胰腺向引流淋巴结的迁移，从而减少胰岛。炎。总之，这些发现确立了异常树突状细胞发育在I型糖尿病中β细胞破坏的起始和消退中的关键作用。

著录项

  • 作者

    Bahjat, Keith S.;

  • 作者单位

    University of Florida.;

  • 授予单位 University of Florida.;
  • 学科 Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2001
  • 页码 93 p.
  • 总页数 93
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 预防医学、卫生学;
  • 关键词

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