Abstract
UV light can be highly beneficial in the treatment of skin disorders such as psoriasis. It is thought to cause immunosuppression by depleting or altering the function of epidermal Langerhans cells (LC). Our previous studies identified a novel langerin(+) dendritic cell in the dermis, distinct from LC in phenotype, circulation, and function. In this study, we determined the role of LC and dermal langerin(+) cells in UV suppression. UV light suppressed the CD8 T cell response to both contact hypersensitivity and epicutaneous protein immunization, and resulted in a dramatically altered phenotype of LC. UV light did not alter early CD8 T cell activation in the lymph nodes, but rather reduced CD8 T cell expansion at later time points. We found that dermal langerin(+) cells, but not LC, were essential for the CD8 T cell response. Furthermore, in the selective absence of LC, UV light still caused suppression of both CD8 T cell expansion and contact hypersensitivity.
Publication types
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Comparative Study
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Research Support, N.I.H., Extramural
MeSH terms
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Administration, Cutaneous
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Animals
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Antigens, Surface / biosynthesis
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CD8-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / transplantation
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Dendritic Cells / immunology
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Dendritic Cells / metabolism
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Dendritic Cells / radiation effects
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Dermatitis, Contact / genetics
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Dermatitis, Contact / immunology
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Dermatitis, Contact / prevention & control
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Epidermal Cells
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Epidermis / immunology*
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Epidermis / metabolism
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Epidermis / radiation effects*
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Gene Knock-In Techniques
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Immunosuppression Therapy / methods*
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Langerhans Cells / immunology*
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Langerhans Cells / metabolism
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Langerhans Cells / radiation effects*
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Lectins, C-Type / biosynthesis
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Mannose-Binding Lectins / biosynthesis
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Mice
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Mice, Inbred C57BL
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Mice, Transgenic
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Ovalbumin / administration & dosage
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Ovalbumin / immunology
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Ultraviolet Rays*
Substances
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Antigens, Surface
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Cd207 protein, mouse
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Lectins, C-Type
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Mannose-Binding Lectins
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Ovalbumin