期刊
MULTIPLE SCLEROSIS JOURNAL
卷 22, 期 12, 页码 1587-1595出版社
SAGE PUBLICATIONS LTD
DOI: 10.1177/1352458515624558
关键词
TREM-2; multiple sclerosis; immunosuppressive therapy; natalizumab; mitoxantrone; cerebrospinal fluid; microglia
资金
- Swedish Federal Government (LUA/ALF agreement)
- Swedish Society of the Neurologically Disabled
- Research Foundation of the Multiple Sclerosis Society of Gothenburg
- Edit Jacobson Foundation
- Biogen
- Swedish Research Council
- Knut and Alice Wallenberg Foundation
- Frimurarestiftelsen
Background: Microglia-mediated proteolysis of the triggering receptor expressed on myeloid cells-2 (TREM-2) produces soluble TREM-2 (sTREM-2) that can be measured in cerebrospinal fluid (CSF) samples. Loss-of-function mutations in TREM2 or in the gene encoding its adaptor protein cause the rare Nasu-Hakola disease (NHD). Multiple sclerosis (MS) is an autoimmune disease that in common with NHD is characterized by demyelination and microglial activation. Objective: To investigate the potential utility of sTREM-2 as a biomarker for MS and to follow treatment effects. Methods: sTREM-2 was analyzed in CSF samples from subjects with MS (N = 59); relapsing-remitting MS (RRMS) (N = 36), secondary progressive MS (SPMS) (N = 20) and primary progressive MS (PPMS) (N = 3), and controls (N = 27). CSF levels of sTREM-2 were also assessed before and after treatment of patients with natalizumab or mitoxantrone. Results: CSF levels of sTREM-2 were significantly increased in patients with RRMS, SPMS, and PPMS compared with controls. After natalizumab treatment, the levels of sTREM-2 were normalized to control levels. The levels of sTREM-2 were also reduced after mitoxantrone treatment. Conclusion: Increased CSF levels of sTREM-2, a new marker of microglial activation, in MS and normalization upon treatment with either natalizumab or mitoxantrone support a role for microglial activation in active MS.
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