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Buchumschlag von TGF-β in Mice Ameliorates Experimental Autoimmune Encephalomyelitis in Regulating NK Cell Activity
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TGF-β in Mice Ameliorates Experimental Autoimmune Encephalomyelitis in Regulating NK Cell Activity

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Bibliographische Detailangaben
Zeitschriftentitel: Cell Transplantation
Personen und Körperschaften: Xu, J., Wang, Y., Jiang, H., Sun, M., Gao, J., Xie, A.
In: Cell Transplantation, 28, 2019, 9-10, S. 1155-1160
Medientyp: E-Article
Sprache: Englisch
veröffentlicht:
SAGE Publications
Schlagwörter:
Transplantation
Cell Biology
Biomedical Engineering
Details
Zusammenfassung: <jats:p> Multiple sclerosis is a disease characterized by inflammation and demyelination located in the central nervous system. Experimental autoimmune encephalomyelitis (EAE) is the most common animal model for multiple sclerosis (MS). Although the roles of T cells in MS/EAE have been well investigated, little is known about the functions of other immune cells in the neuroinflammation model. Here we found that an essential cytokine transforming growth factor β (TGF-β) which could mediate the differentiation of Th17/regulatory T cells was implicated in the natural killer (NK) cells’ activity in EAE. In EAE mice, TGF-β expression was first increased at the onset and then decreased at the peak, but the expressions of TGF-β receptors and downstream molecules were not affected in EAE. When we immunized the mice with MOG antigen, it was revealed that TGF-β treatment reduced susceptibility to EAE with a lower clinical score than the control mice without TGF-β. Consistently, inflammatory cytokine production was reduced in the TGF-β treated group, especially with downregulated pathogenic interleukin-17 in the central nervous system tissue. Furthermore, TGF-β could increase the transcription level of NK cell marker NCR1 both in the spleen and in the CNS without changing other T cell markers. Meanwhile TGF-β promoted the proliferation of NK cell proliferation. Taken together, our data demonstrated that TGF-β could confer protection against EAE model in mice through NK cells, which would be useful for the clinical therapy of MS. </jats:p>
Umfang: 1155-1160
ISSN: 0963-6897
1555-3892
DOI: 10.1177/0963689719852354