RORγt, but not T-bet, overexpression exacerbates an autoimmune model for multiple sclerosis
書誌事項
- 公開日
- 2014-11
- 権利情報
-
- https://www.elsevier.com/tdm/userlicense/1.0/
- https://www.elsevier.com/legal/tdmrep-license
- DOI
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- 10.1016/j.jneuroim.2014.09.006
- 公開者
- Elsevier BV
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説明
Th17 cells play an important role in multiple sclerosis (MS) and its autoimmune model, experimental autoimmune encephalomyelitis (EAE). However, studies have not addressed how enhanced Th17 immune responses can affect demyelinating diseases. We induced EAE with MOG in RORγt transgenic C57BL/6 mice that overexpress a Th17 inducing transcription factor. RORγt transgenic mice developed more severe EAE than wild-type mice with more robust anti-MOG Th17 immune responses. In contrast, mice overexpressing T-bet, a Th1-inducing transcription factor, were resistant to EAE. Therefore, a genetic bias toward Th17 immune responses could contribute to CNS immunopathology.
収録刊行物
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- Journal of Neuroimmunology
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Journal of Neuroimmunology 276 (1-2), 142-149, 2014-11
Elsevier BV
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キーワード
- Central Nervous System
- Encephalomyelitis, Autoimmune, Experimental
- Multiple Sclerosis
- Mice, Transgenic
- Nuclear Receptor Subfamily 1, Group F, Member 3
- Th1 Cells
- Flow Cytometry
- Mice, Inbred C57BL
- Disease Models, Animal
- Mice
- Leukocytes, Mononuclear
- Animals
- T-bet Transcription Factor
- T-Box Domain Proteins
- Cell Proliferation