Abstract
Mice lacking epidermal Langerhans cells (LC) develop exaggerated contact-hypersensitivity (CHS) responses due to the absence of LC during sensitization/initiation. Examination of T cell responses reveals that the absence of LC leads to increased numbers of hapten-specific CD4 and CD8 T cells but does not alter cytokine expression or development of T regulatory cells. CHS responses and Ag-specific T cells are increased in mice in which MHC class II is ablated specifically in LC suggesting that direct cognate interaction between LC and CD4 cells is required for suppression. LC-derived IL-10 is also required for optimal inhibition of CHS. Both LC-derived IL-10-mediated suppression and full LC activation require LC expression of MHC class II. These data support a model in which cognate interaction of LC with CD4 T cells enables LC to inhibit expansion of Ag-specific responses via elaboration of IL-10.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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CD4-Positive T-Lymphocytes / drug effects
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CD4-Positive T-Lymphocytes / immunology*
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CD4-Positive T-Lymphocytes / metabolism
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Cytokines / immunology
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Cytokines / metabolism
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Dermatitis, Contact / immunology*
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Dermatitis, Contact / metabolism
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Dinitrofluorobenzene / immunology
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Dinitrofluorobenzene / pharmacology
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Histocompatibility Antigens Class II / immunology*
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Histocompatibility Antigens Class II / metabolism
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Homeodomain Proteins / genetics
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Homeodomain Proteins / immunology
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Homeodomain Proteins / metabolism
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Inflammation / chemically induced
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Inflammation / immunology
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Inflammation / metabolism
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Interleukin-10 / immunology*
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Interleukin-10 / metabolism
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Langerhans Cells / immunology*
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Langerhans Cells / metabolism
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Mice
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Mice, Mutant Strains
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Skin / immunology
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T-Lymphocytes, Regulatory / immunology*
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T-Lymphocytes, Regulatory / metabolism
Substances
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Cytokines
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Histocompatibility Antigens Class II
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Homeodomain Proteins
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RAG-1 protein
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Interleukin-10
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Dinitrofluorobenzene