α-Synuclein deficiency promotes neuroinflammation by increasing Th1 cell-mediated immune responses

Ettle B, Kuhbandner K, Joerg S, Hoffmann A, Winkler J, Linker R (2016)

Publication Type: Journal article

Publication year: 2016

Journal

Book Volume: 13

Pages Range: 201

Journal Issue: 1

DOI: 10.1186/s12974-016-0694-4

Abstract

Increased ?-synuclein immunoreactivity has been associated with inflammatory activity in multiple sclerosis (MS) lesions, but the function of ?-synuclein in neuroinflammation remains unknown. The aim of this study was to examine the role of ?-synuclein in immunological processes in murine experimental autoimmune encephalomyelitis (EAE) as a model of MS.We studied EAE in wildtype (aSyn(+/+)) and ?-synuclein knockout (aSyn(-/-)) mice on a C57BL/6N background. In the spleen and spinal cord of aSyn(+/+) mice, we observed a gradual reduction of ?-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-?-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.Our findings indicate a functional role of ?-synuclein in early EAE by increasing Th1 cell-mediated immune response.

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APA:

Ettle, B., Kuhbandner, K., Joerg, S., Hoffmann, A., Winkler, J., & Linker, R. (2016). α-Synuclein deficiency promotes neuroinflammation by increasing Th1 cell-mediated immune responses. Journal of Neuroinflammation, 13(1), 201. https://doi.org/10.1186/s12974-016-0694-4

MLA:

Ettle, Benjamin, et al. "α-Synuclein deficiency promotes neuroinflammation by increasing Th1 cell-mediated immune responses." Journal of Neuroinflammation 13.1 (2016): 201.

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