CHARACTERIZATION OF MICROGLIA AND MACROPHAGES IN THE CENTRAL-NERVOUS-SYSTEM OF RATS - DEFINITION OF THE DIFFERENTIAL EXPRESSION OF MOLECULES USING STANDARD AND NOVEL MONOCLONAL-ANTIBODIES IN NORMAL CNS AND IN 4 MODELS OF PARENCHYMAL REACTION
CHARACTERIZATION OF MICROGLIA AND MACROPHAGES IN THE CENTRAL-NERVOUS-SYSTEM OF RATS - DEFINITION OF THE DIFFERENTIAL EXPRESSION OF MOLECULES USING STANDARD AND NOVEL MONOCLONAL-ANTIBODIES IN NORMAL CNS AND IN 4 MODELS OF PARENCHYMAL REACTION
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DOI：
10.1002/glia.440070108
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发表时间：
1993-01-01
期刊：
影响因子：
6.2
通讯作者：
HICKEY, WF
中科院分区：
文献类型：
--
作者：
FLARIS, NA;DENSMORE, TL;HICKEY, WF
本报告描述了一个新的面板的单克隆抗体产生的小鼠与培养的大鼠小胶质细胞免疫。使用这些新试剂和先前定义的与小胶质细胞或巨噬细胞结合的抗体，在4种不同的中枢神经系统反应模型中检查了实质小胶质细胞、血管周围“小胶质”细胞和浸润性巨噬细胞/单核细胞的反应。这些是脑脓肿，实验性变态反应性脑脊髓炎，沃勒变性，刺伤。没有一种新的抗体仅对小胶质细胞具有特异性;所有阳性染色小胶质细胞的抗体也标记了免疫系统正常组织中巨噬细胞/单核细胞的各种亚群。此外，研究结果表明，小胶质细胞能够产生不同水平和各种类型的反应，正如它们所阐述的分子所定义的那样。这些发现表明，这些CNS驻留细胞属于扩展的单核细胞/巨噬细胞/树突状细胞家族，并且它们不会以刻板的方式对所有形式的CNS损伤作出反应。
This report describes the development of a new panel of monoclonal antibodies produced following immunization of mice with cultured rat microglial cells. Using these new reagents and previously defined antibodies that bind to microglia or macrophages, the responses of parenchymal microglia, perivascular ''microglial' cells, and infiltrating macrophage/monocytes were examined in 4 divergent models of central nervous system reaction. These were brain abscess, experimental allergic encephalomyelitis, Wallerian degeneration, and stab wound. No single new antibody was specific only for microglia; all antibodies positively staining microglial cells also labeled various subsets of macrophage/monocytic cells in normal tissues of the immune system. Moreover, the results indicate that microglia are capable of different levels and a variety of types of response, as defined by the molecules they elaborate. These findings suggest that these CNS resident cells belong to the extended monocyte/macrophage/dendritic cell family and that they do not respond in a stereotypic manner to all forms of CNS insult.