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首页> 外文学位 >Roles of CD68 in macrophage function, host defense, atherosclerosis and autoimmunity.
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Roles of CD68 in macrophage function, host defense, atherosclerosis and autoimmunity.

机译：CD68在巨噬细胞功能，宿主防御，动脉粥样硬化和自身免疫中的作用。

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摘要

Murine CD68 (macrosialin) is a plasma membrane protein expressed in macrophages and macrophage-related cells, including langerhans cells, dendritic cells, and osteoclasts. Although the function of CD68 is unknown, it has been postulated to play roles in phagocytosis and cell-pathogen interactions as it is strongly expressed in monocytes and undergoes changes in expression during inflammatory responses. Some studies suggested that CD68 is capable of binding a wide range of ligands, including bacteria pathogens, oxidatively modified low-density lipoprotein (OxLDL), and oxidatively damaged cells. It has also been proposed that it may be involved in antigen presentation. Although CD68 is localized predominantly intracellularly in late endosomes, it exhibits rapid translocation between intracellular membranes and the plasma membrane. Relatively low levels of surface CD68 expression may thus be sufficient for the rapid uptake of various ligands by macrophages. In this study, we generated CD68-deficient mice by gene targeting. The CD68-deficient animals were more susceptible to bacterial infection than the wild type littermates, and macrophages from CD68-deficient mice were defective in bacterial binding and phagocytosis both in vivo and in vitro. In addition, the macrophage binding of oxidatively damaged red blood cell (OxRBC) was dramatically reduced in CD68-deficient mice. These results indicate that CD68 plays a protective role in host defense and that it may function in apoptosis by clearing oxidatively damaged cells. More surprisingly, CD68-deficient mice exhibited evidence of autoimmune diabetes, including pancreatic inflammation, reduced insulin production, and elevated plasma glucose. The CD68-deficient mice also exhibited increased atherosclerosis, elevated levels of auto-antibodies against chromatin and double strand DNA, and infiltration of lymphocytes in multiple tissues such as kidney, lung, and adipose tissue, indicating the development of a murine lupus alike disorder. The CD68 deficient mouse thus provides an excellent model for the investigation of antigen presenting cell (APC) dysfunction and their roles in the development of diseases.
机译：鼠CD68（macrosialin）是在巨噬细胞和巨噬细胞相关细胞（包括朗格汉斯细胞，树突状细胞和破骨细胞）中表达的质膜蛋白。尽管CD68的功能尚不清楚，但据推测它在吞噬作用和细胞-病原体相互作用中发挥作用，因为它在单核细胞中强烈表达并在炎症反应过程中发生表达变化。一些研究表明CD68能够结合多种配体，包括细菌病原体，氧化修饰的低密度脂蛋白（OxLDL）和氧化损伤的细胞。还已经提出它可能与抗原呈递有关。尽管CD68主要位于晚期内体中的细胞内，但它在细胞内膜和质膜之间显示出快速易位。因此，相对较低水平的表面CD68表达可能足以被巨噬细胞快速摄取各种配体。在这项研究中，我们通过基因靶向产生了CD68缺陷型小鼠。缺乏CD68的动物比野生型同窝小鼠更容易受到细菌的感染，来自CD68缺乏的小鼠的巨噬细胞在细菌的结合和吞噬作用方面都存在缺陷，体内和体外。另外，在CD68缺陷型小鼠中，氧化损伤的红细胞（OxRBC）的巨噬细胞结合显着降低。这些结果表明，CD68在宿主防御中起保护作用，并可能通过清除氧化损伤的细胞而在细胞凋亡中起作用。更令人惊讶的是，缺乏CD68的小鼠表现出自身免疫性糖尿病的证据，包括胰腺炎症，胰岛素生成减少和血浆葡萄糖升高。 CD68缺陷型小鼠还表现出动脉粥样硬化增加，针对染色质和双链DNA的自身抗体水平升高以及淋巴细胞在多种组织（例如肾脏，肺和脂肪组织）中的浸润，表明鼠类狼疮样疾病的发展。因此，缺乏CD68的小鼠为研究抗原呈递细胞（APC）功能障碍及其在疾病发展中的作用提供了一个极好的模型。

著录项

  • 作者

    Jiang, Zhiming.;

  • 作者单位

    University of California, Los Angeles.;

  • 授予单位 University of California, Los Angeles.;
  • 学科 Biology Microbiology.; Biology Molecular.; Health Sciences Immunology.
  • 学位 Ph.D.
  • 年度 2001
  • 页码 185 p.
  • 总页数 185
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 微生物学;分子遗传学;预防医学、卫生学;
  • 关键词

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