Microglia suppress the secondary progression of autoimmune encephalomyelitis

被引：41

作者：

Tanabe, Shogo ^{[1
,2
]}

Saitoh, Shohei ^{[2
]}

Miyajinna, Hisao ^{[2
,4
]}

Itokazu, Takahide ^{[2
,3
]}

Yannashita, Toshihide ^{[1
,2
,3
,4
]}

机构：

[1] Osaka Univ, Frontier Res Ctr, Dept Mol Neurosci, World Premier Int,Immunol, 3-1 Yamadaoka, Suita, Osaka 5650871, Japan

[2] Osaka Univ, Grad Sch Med, Dept Mol Neurosci, Suita, Osaka, Japan

[3] Osaka Univ, Grad Sch Med, Dept Neuromed Sci, Suita, Osaka, Japan

[4] Osaka Univ, Grad Sch Frontier Biosci, Suita, Osaka, Japan

来源：

GLIA | 2019年 / 67卷 / 09期

关键词：

microglia; neuro-immune interactions; PLX3397; secondary progressive multiple sclerosis; T cell; STIMULATING FACTOR-1 RECEPTOR; MULTIPLE-SCLEROSIS; NEURONAL LOSS; AXONAL LOSS; CELLS; EXPRESSION; MONOCYTES; ACTIVATION; DAMAGE;

D O I：

10.1002/glia.23640

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Secondary progressive multiple sclerosis (SPMS) is an autoimmune disease of the central nervous system (CNS) characterized by progressive motor dysfunction, sensory deficits, and visual problems. The pathological mechanism of SPMS remains poorly understood. In this study, we investigated the role of microglia, immune cells in the CNS, in a secondary progressive form of experimental autoimmune encephalomyelitis (EAE), the mouse model of SPMS. We induced EAE in nonobese diabetic mice and treated the EAE mice with PLX3397, an antagonist of colony stimulating factor-1 receptor, during secondary progression in order to deplete microglia. The results showed that PLX3397 treatment significantly exacerbated secondary progression of EAE and increased mortality rates. Additionally, histological analysis showed that PLX3397 treatment significantly promoted inflammation, demyelination, and axonal degeneration. Moreover, the number of CD4(+) T cells in the spinal cord of EAE mice was expanded due to PLX3397-mediated proliferation. These results suggest that microglia suppressed secondary progression of EAE by inhibiting the proliferation of CD4(+) T cells in the CNS.

引用

页码：1694 / 1704

页数：11

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