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Contact Hypersensitivity as a Murine Model of Allergic Contact Dermatitis
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Langerhans cells suppress contact hypersensitivity responses via cognate CD4 interaction and langerhans cell-derived

Botond Z Igyarto1, Matthew C Jenison, Jan C Dudda

  • 1Department of Dermatology, Center for Immunology, University of Minnesota, Minneapolis, MN 55455, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|October 6, 2009
PubMed

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.

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