期刊
MUCOSAL IMMUNOLOGY
卷 4, 期 4, 页码 438-447出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/mi.2010.91
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资金
- Swedish Medical Research Council
- Swedish National Health Service
- Crafoordska Foundation
- Torsten and Ragnar Soderbergs Foundation
- Kocks Foundation
- Osterlund and Richard Foundation
- Ruth Julins Foundation
- Royal Physiographic Society
- Wellcome Trust
- Swedish foundation for Strategic Research
Small intestinal lamina propria (SI-LP) CD103(+) dendritic cells (DCs) are imprinted with an ability to metabolize vitamin A (retinol), a property underlying their enhanced capacity to induce the gut-homing receptors CC chemokine receptor-9 and alpha 4 beta 7 on responding T cells. In this study, we demonstrate that imprinting of CD103(+) DCs is itself critically dependent on vitamin A and occurs locally within the small intestine (SI). The major vitamin A metabolite retinoic acid (RA) induced retinol-metabolizing activity in DCs both in vitro and in vivo, suggesting a direct role for RA in this process. Consistent with this, SI-LP CD103(+) DCs constitutively received RA signals in vivo at significantly higher levels than did colonic CD103(+) DCs. Remarkably, SI CD103(+) DCs remained imprinted in mice depleted of dietary but not of systemic retinol. We found that bile contained high levels of retinol, induced RA receptor-dependent retinol-metabolizing activity in bone marrow-derived DCs, and imprinted these cells with the ability to generate gut-tropic T cells. Taken together, these results suggest a novel and unexpected role for bile in SI-LP CD103(+) DC imprinting.
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