Clinical Immunology, University Hospital Zurich, Häldeliweg 4, CH-8044 Zürich, Switzerland.
Brain. 2011 May;134(Pt 5):1315-30. doi: 10.1093/brain/awr070.
Increased expression of the chondroitin proteoglycan NG2 is a prominent feature in central nervous system injury with unknown cellular source and biological relevance. Here, we describe the first detailed analysis of experimental autoimmune encephalomyelitis in NG2 knockout mice and NG2 knockout bone marrow chimeras. We show that both macrophages and oligodendrocyte progenitor cells express and secrete NG2 in response to transforming growth factor-β. A subpopulation of macrophages expresses NG2 within leucocyte infiltrates in the central nervous system, but only oligodendrocyte progenitor cells contribute to NG2 accumulation. Notably, NG2 plays no role in experimental autoimmune encephalomyelitis initiation, progression or recuperation. In concurrence, the immune response is unaltered in NG2-deficient mice as are the extent of central nervous system damage and degree of remyelination.
神经胶质细胞源性硫酸软骨素蛋白多糖 NG2 的表达增加是中枢神经系统损伤的一个显著特征，但细胞来源和生物学相关性尚不清楚。在这里，我们描述了在 NG2 基因敲除小鼠和 NG2 基因敲除骨髓嵌合体中实验性自身免疫性脑脊髓炎的首次详细分析。我们表明，转化生长因子-β 可诱导巨噬细胞和少突胶质前体细胞表达和分泌 NG2。在中枢神经系统白细胞浸润中，巨噬细胞的一个亚群表达 NG2，但只有少突胶质前体细胞有助于 NG2 的积累。值得注意的是，NG2 对实验性自身免疫性脑脊髓炎的起始、进展或恢复没有作用。同时，NG2 缺失小鼠的免疫反应没有改变，中枢神经系统损伤的程度和髓鞘再生的程度也没有改变。
