| Author |
Braun, Andrea Dewert, Nadin Brunnert, Fiona Schnabel, Viktor Hardenberg, Jan-Hendrik Richter, Beatrice Zachmann, Karolin Cording, Sascha Claßen, Anna Brans, Richard Hamann, Alf Huehn, Jochen Schön, Michael P. |
| Description |
Country affiliation: Germany Author Affiliation: Braun A ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Dewert N ( Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany.); Brunnert F ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Schnabel V ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Hardenberg JH ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Richter B ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Zachmann K ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Cording S ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Claßen A ( Experimental Rheumatology, German Rheumatism Research Center Berlin and Charité University Medicine Berlin, Campus Mitte, Berlin, Germany.); Brans R ( Department of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.); Hamann A ( Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany.); Huehn J ( Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany.); Schön MP ( Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany.) |
| Abstract |
Murine contact hypersensitivity (CHS) is a dendritic cell (DC)-dependent T-cell-mediated inflammation with CD8+ T cells as effectors and CD4+ T cells as regulators (Treg cells) that models human allergic contact dermatitis. The integrin E(CD103) is expressed by some T-cell and DC subsets and has been implicated in epithelial lymphocyte localization, but its role in immune regulation remains enigmatic. We have identified a function for CD103 in the development of cutaneous allergic immune responses. CHS responses, but not irritant contact dermatitis, were significantly augmented in CD103-deficient mice in hapten-challenged skin. Phenotype and function of skin DCs during sensitization were normal, whereas adoptive transfer experiments revealed that the elevated CHS response in CD103-deficient mice is transferred by primed T cells and is independent of resident cells in recipient mice. While T-cell counts were elevated in challenged skin of CD103-deficient mice, the FoxP3 expression level of CD4+CD25+ Treg cells was significantly reduced, indicating impaired functionality. Indeed, Treg cells from CD103-deficient mice were not able to suppress CHS reactions during the elicitation phase. Further, CD103 on FoxP3+ Treg cells was involved in Treg retention to inflamed skin. These findings indicate an unexpected dichotomous functional role for CD103 on Treg cells by modulating FoxP3 expression. |
