期刊
JOURNAL OF IMMUNOLOGY
卷 200, 期 1, 页码 119-129出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1701056
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资金
- Japan Society for the Promotion of Science [26670192, 17K19568, 16K15259]
- Ministry of Education, Culture, Sports, Science and Technology [17H05798]
- Nagoya City University
- Novartis Foundation (Japan) for the Promotion of Science
- Japanese Diabetes Foundation
- Ichihara International Scholarship Foundation
- Minako Shiokawa Yong Investigator's Award for Collagen Disease Research
- Japan Rheumatism Foundation
- Kobayashi Cancer Foundation
- Toyoaki Scholarship Foundation
- Daiko Foundation
- [16H05177]
- [17H4088]
- [17H04242]
- Grants-in-Aid for Scientific Research [16K08704, 16H05177, 15K08431, 17H05798, 17K19568, 16K15259, 15H04744, 17K11679, 26670192, 16K15376, 17H04242] Funding Source: KAKEN
Skin dendritic cells (DCs) are divided into several subsets with distinctive functions. This study shows a previously unappreciated role of dermal CD11b-type Langerin 2 DCs in maintaining immunological self-tolerance after UVB exposure. After UVB exposure, dermal CD11b-type Langerin 2 DCs upregulated surface CD86 expression, induced proliferation of Foxp3(+) regulatory T (Treg) cells without exogenous Ags, and upregulated a set of genes associated with immunological tolerance. This Treg-expansion activity was significantly hampered by CD80/CD86 blockade in vivo. These results indicate that CD11b-type Langerin 2 DCs from the UVB-exposed skin are specialized to expand Treg cells in the skin, which suppress autoimmunity.
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