Disruption of the β2-integrin CD11d(αDβ2) gene fails to protect against experimental autoimmune encephalomyelitis
Disruption of the β2-integrin CD11d(αDβ2) gene fails to protect against experimental autoimmune encephalomyelitis
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DOI：
10.1016/j.jneuroim.2006.12.007
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发表时间：
2007-03-01
影响因子：
3.3
通讯作者：
Barnum, Scott R.
中科院分区：
文献类型：
--
作者：
Adams, Jillian E.;Webb, Matthew S.;Barnum, Scott R.
粘附分子的β（2）-整联蛋白家族的第四个成员CD 11 d（alpha（D）beta（2））在多种免疫细胞上表达，然而其在自身免疫性疾病（包括EAE）中的功能仍然未知。我们使用髓鞘少突胶质细胞糖蛋白（MOG（35-55））肽在野生型和CD 11 d（-/-）C57 BL/6小鼠中诱导EAE。在整个病程中，两组小鼠EAE的临床病程和组织病理学相同。白细胞亚群向中枢神经系统的浸润或从两组小鼠的脾或脊髓分离的T细胞产生的细胞因子无显著差异。我们的数据表明，CD 11 d不是EAE发展所必需的，迄今为止，它是唯一的β（2）-整联蛋白分子，其缺失不会导致减毒疾病。(c)2006 Elsevier B. V.保留所有权利。
The fourth member of the beta(2)-integrin family of adhesion molecules, CD11d (alpha(D)beta(2)), is expressed on a wide variety of immune cells, however its function in autoimmune diseases, including EAE remains unknown. We induced EAE in wild-type and CD11d(-/-) C57BL/6 mice using myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide. The clinical course and histopathology of EAE were identical in both groups of mice throughout the disease course. There were no significant differences in the infiltration of leukocyte subsets into the central nervous system or in the production of cytokines from T cells isolated from the spleen or spinal cord from both groups of mice. Our data demonstrate that CD11d is not required for the development of EAE and, to date, is the only beta(2)-integrin molecule whose deletion does not result in attenuated disease. (c) 2006 Elsevier B.V. All rights reserved.