| First Author | Braun A | Year | 2015 |
| Journal | J Invest Dermatol | Volume | 135 |
| Issue | 12 | Pages | 2982-2991 |
| PubMed ID | 26203637 | Mgi Jnum | J:227569 |
| Mgi Id | MGI:5701573 | Doi | 10.1038/jid.2015.287 |
| Citation | Braun A, et al. (2015) Integrin alphaE(CD103) Is Involved in Regulatory T-Cell Function in Allergic Contact Hypersensitivity. J Invest Dermatol 135(12):2982-91 |
| abstractText | 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 alphaE(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. |
