期刊
NATURE IMMUNOLOGY
卷 8, 期 3, 页码 285-293出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1433
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资金
- NIAID NIH HHS [R01 AI072618, T32 AI007290, 5 T32 AI07290-21] Funding Source: Medline
During adaptive immune responses, dendritic cells activate T cells and endow them with specific homing properties. Mechanisms that 'imprint' specific tropisms, however, are not well defined. We show here that 1,25(OH) D-2(3), the active form of vitamin D3, signaled T cells to express CC chemokine receptor 10, which enabled them to migrate to the skin-specific chemokine CCL27 secreted by keratinocytes of the epidermis. In contrast, 1,25(OH)(2)D-3 suppressed the gut-homing receptors alpha 4 beta 7 and CCR9. Vitamin D3, the inactive prohormone naturally generated in the skin by exposure to the sun, was processed by dendritic cells and T cells to the active metabolite, providing a mechanism for the local regulation of T cell 'epidermotropism'. Our findings support a model in which dendritic cells process and 'interpret' locally produced metabolites to 'program' T cell homing and microenvironmental positioning.
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