Elevated expression of granulocyte-macrophage colony-stimulating factor receptor in multiple sclerosis lesions.
Elevated expression of granulocyte-macrophage colony-stimulating factor receptor in multiple sclerosis lesions.
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DOI：
10.1016/j.jneuroim.2017.12.017
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发表时间：
2018-04-15
影响因子：
3.3
通讯作者：
Rostami A
中科院分区：
文献类型：
--
作者：
Imitola J;Rasouli J;Watanabe F;Mahajan K;Sharan AD;Ciric B;Zhang GX;Rostami A
多发性硬化症（MS）是一种慢性炎症性脱髓鞘和神经退行性疾病，不成比例地影响年轻人，导致残疾和社会成本高。T细胞和单核细胞向中枢神经系统（CNS）的浸润对于疾病的发生和进展至关重要。然而，尽管做了大量的努力，免疫细胞在MS中启动和维持CNS损伤的分子机制尚未阐明。在实验性自身免疫性脑脊髓炎（EAE）中，由致病性Th 1和Th 17细胞产生的粒细胞-巨噬细胞集落刺激因子（GM-CSF）在疾病的初始阶段对于单核细胞向CNS中的募集至关重要。我们和其他人最近表明，与健康个体相比，MS患者具有更多数量的产生GM-CSF的CD 4+和CD 8 + T细胞。在这里，我们描述的表达GM-CSF及其受体，GM-CSFR，在正常脑和MS病变。我们的数据表明，在急性和慢性MS病变，小胶质细胞和星形胶质细胞的GM-CSFR的表达上调，此外，我们表明，GM-CSF相关分子也上调MS病变。这些发现进一步加强了GM-CSF信号转导有助于MS发病机制的论点。
Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease that disproportionately affects young adults, leading to disability and high costs to society. Infiltration of T cells and monocytes into the central nervous system (CNS) is critical for disease initiation and progression. However, despite a great deal of effort the molecular mechanisms by which immune cells initiate and perpetuate CNS damage in MS have not yet been elucidated. In experimental autoimmune encephalomyelitis (EAE), an animal model of MS, granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by pathogenic Th1 and Th17 cells is critical for the recruitment of monocytes into the CNS during the initial stage of disease. We and others have recently shown that, compared with healthy individuals, MS patients have greater numbers of CD4+ and CD8+ T cells that produce GM-CSF. Here, we describe the expression of GM-CSF and its receptor, GM-CSFR, in normal brain and MS lesions. Our data show that in acute and chronic MS lesions, microglia and astrocytes have upregulated expression of GM-CSFR; in addition, we show that GM-CSF-associated molecules are also upregulated in MS lesions. These findings further strengthen the argument that GM-CSF signaling contributes to MS pathogenesis.
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影响因子：
11.2
作者：
Wang, Yue;Imitola, Jaime;Rasmussen, Stine;O'Connor, Kevin C.;Khoury, Samia J.
通讯作者：
Khoury, Samia J.
影响因子：
82.9
作者：
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影响因子：
32.4
作者：
Croxford, Andrew L.;Lanzinger, Margit;Becher, Burkhard
通讯作者：
Becher, Burkhard
影响因子：
3.3
作者：
Comabella, M;Imitola, J;Khoury, SJ
通讯作者：
Khoury, SJ
影响因子：
5.4
作者：
Vogel, Daphne Y. S.;Kooij, Gijs;Dijkstra, Christine D.
通讯作者：
Dijkstra, Christine D.