書誌事項
- 公開日
- 2006-07-30
- 権利情報
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- http://www.springer.com/tdm
- DOI
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- 10.1038/ni1370
- 公開者
- Springer Science and Business Media LLC
この論文をさがす
説明
T cells expressing an invariant V(alpha)19-J(alpha)33 T cell receptor alpha-chain (V(alpha)19i TCR) are restricted by the nonpolymorphic major histocompatibility complex class Ib molecule MR1. Whether V(alpha)19i T cells are involved in autoimmunity is not understood. Here we demonstrate that T cells expressing the V(alpha)19i TCR transgene inhibited the induction and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Similarly, EAE was exacerbated in MR1-deficient mice, which lack V(alpha)19i T cells. EAE suppression was accompanied by reduced production of inflammatory mediators and increased secretion of interleukin 10. Interleukin 10 production occurred at least in part through interactions between B cells and V(alpha)19i T cells mediated by the ICOS costimulatory molecule. These results suggest an immunoregulatory function for V(alpha)19i T cells.
収録刊行物
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- Nature Immunology
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Nature Immunology 7 (9), 987-994, 2006-07-30
Springer Science and Business Media LLC
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キーワード
- Antigens, Differentiation, T-Lymphocyte
- B-Lymphocytes
- Encephalomyelitis, Autoimmune, Experimental
- Multiple Sclerosis
- Receptors, Antigen, T-Cell, alpha-beta
- Histocompatibility Antigens Class I
- Immunoglobulin Variable Region
- Mice, Transgenic
- Lymphocyte Activation
- T-Lymphocytes, Regulatory
- Interleukin-10
- Antigens, CD1
- Inducible T-Cell Co-Stimulator Protein
- Minor Histocompatibility Antigens
- Mice
- Animals
- Antigens, CD1d
詳細情報 詳細情報について
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- CRID
- 1362825896284500352
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- NII論文ID
- 80018933412
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- DOI
- 10.1038/ni1370
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- ISSN
- 15292916
- 15292908
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- PubMed
- 16878136
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- データソース種別
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- Crossref
- CiNii Articles
- OpenAIRE
