Article abstract
Nature Immunology 8, 285 - 293 (2007)
Published online: 28 January 2007 | doi:10.1038/ni1433
DCs metabolize sunlight-induced vitamin D3 to 'program' T cell attraction to the epidermal chemokine CCL27
Hekla Sigmundsdottir1,2,4, Junliang Pan1,2,4, Gudrun F Debes1,2, Carsten Alt1,2, Aida Habtezion1,2, Dulce Soler3 & Eugene C Butcher1,2
Abstract
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)2D3, 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)2D3 suppressed the gut-homing receptors 
4
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.
- Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.
- The Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA.
- Millennium Pharmaceuticals, Cambridge, Massachusetts 02139, USA.
- These authors contributed equally to this work.
Correspondence to: Eugene C Butcher1,2 e-mail: ebutcher@stanford.edu
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