Dendritic cells are abundant in non-lesional gray matter in multiple sclerosis
Dendritic cells are abundant in non-lesional gray matter in multiple sclerosis
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DOI：
10.1016/j.yexmp.2007.05.006
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发表时间：
2007-10-01
影响因子：
3.6
通讯作者：
Rus, Horea
中科院分区：
文献类型：
--
作者：
Cudrici, Cornelia;Ito, Takahiro;Rus, Horea
我们分析了树突状细胞（DC）在非病变灰质（NLGM）与非病变白色物质（NLWM）和急性或慢性活动性多发性硬化（MS）病变中的定位。在冷冻切片上进行免疫组织化学，以检测DC标志物（CD209、CD205、CD83）和炎性细胞的其他标志物（CD68、CD8、CD4、CD3、CCR 7、CCR 5）。我们发现在NLGM的血管周围和实质区域都有表达CD209和含有髓鞘碱性蛋白的细胞。我们的研究结果显示，CD209（+）细胞在NLGM实质区域的表达是令人惊讶的，相对于以前的文献报道，CD209（+）DC的存在，仅在MS斑块血管周围区域。虽然数量少于CD209（+）细胞，但表达成熟DC标记物CD205的NLGM细胞在大多数病变的血管周围袖中一致地检测到。双重标签专家。部分但不是全部的CD209（+）细胞也表达CD68和CCR 5。我们还发现CD 209 T细胞与CD 3（+）淋巴细胞密切接触，这表明DC可能有助于NLGM中病原性T细胞的局部激活。由于NLGM损伤是与残疾累积相关的关键因素之一，靶向DC可能代表MS中预防疾病进展的可能的新治疗方法。(c)2007爱思唯尔公司All rights reserved.
We have analyzed the localization of dendritic cells (DCs) in non-lesional gray matter (NLGM) in comparison to non-lesional white matter (NLWM) and acute or chronic active multiple sclerosis (MS) lesions. Immunohistochemistry was performed on cryostat sections for DCs markers (CD209, CD205, CD83) and other markers for inflammatory cells (CD68, CD8, CD4, CD3, CCR7, CCR5). We found cells expressing CD209 and containing myelin basic protein in both perivascular and parenchymal areas of NLGM. Our findings showing the expression of CD209(+) cells in NLGM parenchymal areas are surprising relative to the previous literature which reported the presence of CD209(+) DCs only in MS plaque perivascular areas. Although less numerous than CD209(+) cells, NLGM cells expressing mature DCs marker CD205 were consistently detected in perivascular cuffs of most lesions. In double labeling expert. ments, some but not all of the CD209(+) cells also expressed CD68 and CCR5. We also found CD209 T cells in close contact with CD3(+) lymphocytes suggesting that DCs might contribute to the local activation of pathogenic T cells in the NLGM. Since injury to the NLGM is one of the key factors associated with disability accumulation, targeting DCs may represent a possible new therapeutic approach in MS to prevent disease progression. (c) 2007 Elsevier Inc. All rights reserved.