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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Phosphatidylserine receptor Tim-4 is essential for the maintenance of the homeostatic state of resident peritoneal macrophages
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Phosphatidylserine receptor Tim-4 is essential for the maintenance of the homeostatic state of resident peritoneal macrophages

机译：磷脂酰丝氨酸受体Tim-4对于维持常驻腹膜巨噬细胞的稳态至关重要

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摘要

Tim-4 is a phosphatidylserine (PS) receptor that is expressed on various macrophage subsets. It mediates phagocytosis of apoptotic cells by peritoneal macrophages. The in vivo functions of Tim-4 in phagocytosis and immune responses, however, are still unclear. In this study, we show that Tim-4 quickly forms punctate caps on contact with apoptotic cells, in contrast to its normal diffused expression on the surface of phagocytes. Despite its expression in marginal zone and tingible body macrophages, Tim-4 deficiency only minimally affects outcomes of several acute immune challenges, including the trapping of apoptotic cells in the marginal zone, the clearance apoptotic cells by tingible body macrophages, and the formation of germinal centers and elicitation of antibody responses against sheep red blood cells (SRBCs). In addition, Tim-4~(-/-) resident peritoneal macrophages (rPMs) phagocytose necrotic cells and other opsonized targets normally. However, their ability to bind and engulf apoptotic cells is significantly compromised both in vitro and in vivo. Most importantly, Tim-4 deficiency results in increased cellularity in the peritoneum. Resting rPMs produce higher TNF-α in culture. Their response to LPS, on the contrary, is dampened. Our data support an indispen-sible role of Tim-4 in maintaining the homeostasis of rPMs.
机译：Tim-4是在各种巨噬细胞亚群上表达的磷脂酰丝氨酸（PS）受体。它通过腹膜巨噬细胞介导凋亡细胞的吞噬作用。然而，尚不清楚Tim-4在吞噬作用和免疫反应中的体内功能。在这项研究中，我们表明Tim-4在与凋亡细胞接触时迅速形成点状帽，这与吞噬细胞表面的正常扩散表达相反。尽管其在边缘区和可染性巨噬细胞中表达，Tim-4缺乏仅对几种急性免疫挑战的结果产生最小的影响，包括在边缘区中捕获凋亡细胞，可食用性巨噬细胞清除凋亡细胞以及生发的形成。中心和对绵羊红细胞（SRBC）的抗体应答的诱导。另外，Tim-4〜（-/-）常驻性腹膜巨噬细胞（rPM）吞噬坏死细胞和其他调理靶。然而，它们结合和吞噬凋亡细胞的能力在体外和体内均显着受损。最重要的是，Tim-4缺乏症导致腹膜细胞增多。静止的rPM在培养中产生更高的TNF-α。相反，它们对脂多糖的反应减弱了。我们的数据支持Tim-4在维持rPM稳态方面的不可或缺的作用。

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  • 作者

    Kit Wong; Patricia A. Valdez; Christine Tan; Sherry Yeh; Jo-Anne Hongo; Wenjun Ouyang;

  • 作者单位

    Departments of Immunology, Genentech, Inc., South San Francisco, CA 94080;

    Departments of Immunology, Genentech, Inc., South San Francisco, CA 94080 Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892;

    Departments of Antibody Engineering, Genentech, Inc., South San Francisco, CA 94080;

    Departments of Assay and Automation Technology, Genentech, Inc., South San Francisco, CA 94080;

    Departments of Antibody Engineering, Genentech, Inc., South San Francisco, CA 94080;

    Departments of Immunology, Genentech, Inc., South San Francisco, CA 94080;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    phagocytosis; apoptotic cells; receptor dynamics; TNF-α;

    机译：吞噬作用凋亡细胞;受体动力学;肿瘤坏死因子-α;

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