Chemokine production by rat myocytes exposed to interferon-γ
Chemokine production by rat myocytes exposed to interferon-γ
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DOI：
10.1006/clim.1999.4828
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发表时间：
2000-02-01
影响因子：
8.6
通讯作者：
Krolick, KA
中科院分区：
文献类型：
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作者：
Reyes-Reyna, SM;Krolick, KA
编码单核细胞趋化蛋白-1(MCP-1)的信使RNA及其蛋白产物在单克隆性Lewis大鼠骨骼肌细胞系(LEI)中呈低水平结构性表达，对骨骼肌切片的免疫组织化学分析也得到了类似的结果。由于干扰素-γ被报道在确定神经肌肉自身免疫性疾病实验性重症肌无力(EAMG)的症状严重程度中可能起作用，在这些研究中验证并被证明是正确的假设是，干扰素-γ将上调LE1细胞中MCP-I的产生。还观察到，肌源性MCP-1在接受抗乙酰胆碱受体单抗(MAb35)的大鼠体内可以上调，mAb35是EAMG症状的有效诱导剂。因此，可以得出结论，肌肉可能通过产生影响免疫系统活动的因素来促进疾病的进展。(C)2000年学术出版社。
Messenger RNA that encodes for monocyte chemotactic protein-1 (MCP-1), as well as its protein product, was observed to be constitutively expressed at low levels in a monoclonal Lewis rat skeletal muscle cell line (LEI), Immunohistochemical analyses of sections of skeletal muscle yielded similar results. Since interferon-gamma (IFN-gamma) has been reported to have a likely role in determining the severity of symptoms in the neuromuscular autoimmune disease experimental myasthenia gravis (EAMG), the hypothesis tested and proven true in these studies was that IFN-gamma would up-regulate the production of MCP-I in LE1 cells. It was also observed that muscle-derived MCP-1 could be up-regulated in vivo in rats receiving a monoclonal anti-acetylcholine receptor antibody (mAb35), a potent inducer of symptoms of EAMG. Therefore, it is concluded that muscle may contribute to disease progression by producing factors that influence activities of the immune system. (C) 2000 Academic Press.