期刊
NATURE IMMUNOLOGY
卷 12, 期 12, 页码 1184-U77出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2135
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资金
- US National Institutes of Health
- Crohn's and Colitis Foundation of America
- Damon Runyon Cancer Research Foundation
- Kenneth Rainin Foundation
- UCSF Liver Center
- Wellcome Trust [076113, 085475]
Dendritic cells (DCs), which are known to support immune activation during infection, may also regulate immune homeostasis in resting animals. Here we show that mice lacking the ubiquitin-editing molecule A20 specifically in DCs spontaneously showed DC activation and population expansion of activated T cells. Analysis of DC-specific epistasis in compound mice lacking both A20 and the signaling adaptor MyD88 specifically in DCs showed that A20 restricted both MyD88-independent signals, which drive activation of DCs and T cells, and MyD88-dependent signals, which drive population expansion of T cells. In addition, mice lacking A20 specifically in DCs spontaneously developed lymphocyte-dependent colitis, seronegative ankylosing arthritis and enthesitis, conditions stereotypical of human inflammatory bowel disease (IBD). Our findings indicate that DCs need A20 to preserve immune quiescence and suggest that A20-dependent DC functions may underlie IBD and IBD-associated arthritides.
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