| Autor: |
Ettle, Benjamin, Kuhbandner, Kristina, Jörg, Stefanie, Hoffmann, Alana, Winkler, Jürgen, Linker, Ralf A. |
| Jazyk: |
angličtina |
| Předmět: |
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| Zdroj: |
Journal of Neuroinflammation. 13(1) |
| ISSN: |
1742-2094 |
| DOI: |
10.1186/s12974-016-0694-4 |
| Popis: |
Background Increased α-synuclein immunoreactivity has been associated with inflammatory activity in multiple sclerosis (MS) lesions, but the function of α-synuclein in neuroinflammation remains unknown. The aim of this study was to examine the role of α-synuclein in immunological processes in murine experimental autoimmune encephalomyelitis (EAE) as a model of MS. Findings We studied EAE in wildtype (aSyn+/+) and α-synuclein knockout (aSyn−/−) mice on a C57BL/6N background. In the spleen and spinal cord of aSyn+/+ mice, we observed a gradual reduction of α-synuclein expression during EAE, starting already in the pre-symptomatic disease phase. Compared to aSyn+/+ mice, aSyn−/− mice showed an earlier onset of symptoms but no differences in symptom severity at the peak of disease. Earlier symptom onset was accompanied by increased spinal cord infiltration of CD4+ T cells, predominantly of interferon-γ-producing T helper 1 (Th1) cells, and reduced infiltration of regulatory T cells, whereas antigen-presenting cells were unaltered. Pre-symptomatically, aSyn−/− mice exhibited hyperproliferative CD4+ splenocytes consistent with increased splenic interleukin-2 mRNA expression, resulting in increased numbers of Th1 cells in the spleen at the onset of symptoms. Conclusions Our findings indicate a functional role of α-synuclein in early EAE by increasing Th1 cell-mediated immune response. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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