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首页> 外文学位 >The absence of CD62L (L-selectin) does not inhibit the progression of autoimmune diabetes in nonobese diabetic (NOD) mice.
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The absence of CD62L (L-selectin) does not inhibit the progression of autoimmune diabetes in nonobese diabetic (NOD) mice.

机译：在非肥胖糖尿病（NOD）小鼠中，CD62L（L-选择素）的缺乏不会抑制自身免疫性糖尿病的进展。

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摘要

Insulin dependent diabetes mellitus (IDDM) results from an autoreactive immune response targeting the insulin producing β cells found in the islets of Langerhans in the pancreas. Diabetogenesis depends on β cell-reactive T cells trafficking to the islets of Langerhans and effecting β cell destruction. The nonobese diabetic (NOD) mouse spontaneously develops autoimmune diabetes and serves as an excellent model for investigating the immunological processes involved in β cell autoimmunity.; Leukocyte trafficking relies on distinct families of adhesion molecules that regulate tissue-specific homing to secondary lymphoid organs and sites of inflammation. Extravasation begins with the rolling of leukocytes along the endothelial wall and occurs through leukocyte-endothelial cell interactions mediated by the selectin family. One member of the selectin family, CD62L (L selectin), is expressed on virtually all leukocytes and is critical for the efficient population of peripheral lymph nodes, homing to inflamed tissues, and the generation of primary T cell responses.; We and others have previously shown that administration of monoclonal antibodies directed against CD62L can reduce insulitis and prevent diabetes in NOD mice. Prevention is most effective when treatment is begun at an early age, suggesting a crucial role for CD62L in the initial recruitment of T cells to the pancreas and establishment of insulitis.; To further examine the role of CD62L in the development of IDDM, NOD mice with a disrupted CD62L gene were established. The lack of CD62L had no apparent effect on the time of onset or frequency of diabetes. Furthermore, T cell activation, homing, and β cell-specific reactivity in CD62L −/− mice were similar to CD62L+/+ mice. We also evaluated the importance of CD62L in a CD4+ transgenic T cell adoptive transfer model of diabetes. No discernible difference in homing to the pancreatic lymph nodes or induction of diabetes was observed in the absence of CD62L. We conclude that CD62L is not absolutely required for the development of IDDM in NOD mice.
机译：胰岛素依赖型糖尿病（IDDM）是由针对胰腺胰岛Langerhans胰岛中产生胰岛素的β细胞的自身反应性免疫反应产生的。糖尿病的发生取决于β细胞反应性T细胞向胰岛的运输，并影响β细胞的破坏。非肥胖糖尿病（NOD）小鼠自发发展为自身免疫性糖尿病，并且是研究与β细胞自身免疫有关的免疫过程的出色模型。白细胞运输依赖于不同的粘附分子家族，这些家族调节着组织特异性归巢至次级淋巴器官和炎症部位。外渗始于白细胞沿内皮壁的滚动，并通过选择素家族介导的白细胞-内皮细胞相互作用而发生。选择素家族的一个成员CD62L（L选择素）几乎在所有白细胞上表达，对于有效的周围淋巴结聚集，归巢到发炎的组织以及原代T细胞反应的产生至关重要。我们和其他人以前已经表明，针对CD62L的单克隆抗体的施用可以减少NOD小鼠的胰岛炎并预防糖尿病。当预防从小就开始时，预防是最有效的，这表明CD62L在T细胞最初募集到胰腺和建立胰岛炎中起着至关重要的作用。为了进一步检查CD62L在IDDM发育中的作用，建立了CD62L基因被破坏的NOD小鼠。 CD62L的缺乏对糖尿病的发作时间或频率没有明显影响。此外，CD62L -/-小鼠的T细胞活化，归巢和β细胞特异性反应与CD62L + / + 小鼠相似。我们还评估了CD62L在糖尿病CD4 + 转基因T细胞过继转移模型中的重要性。在没有CD62L的情况下，归巢至胰腺淋巴结或诱发糖尿病方面没有明显差异。我们得出结论，在NOD小鼠中IDDM的发育并非绝对需要CD62L。

著录项

  • 作者

    Friedline, Randall Henry.;

  • 作者单位

    The University of North Carolina at Chapel Hill.;

  • 授予单位 The University of North Carolina at Chapel Hill.;
  • 学科 Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2001
  • 页码 171 p.
  • 总页数 171
  • 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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