| First Author | Bruhs A | Year | 2018 |
| Journal | J Invest Dermatol | Volume | 138 |
| Issue | 3 | Pages | 570-579 |
| PubMed ID | 29045819 | Mgi Jnum | J:258434 |
| Mgi Id | MGI:6117996 | Doi | 10.1016/j.jid.2017.09.032 |
| Citation | Bruhs A, et al. (2018) Disruption of the Epidermal Barrier Induces Regulatory T Cells via IL-33 in Mice. J Invest Dermatol 138(3):570-579 |
| abstractText | Disturbance of the epidermal barrier by UVR is associated with the release of antimicrobial peptides and inflammatory cytokines for the purpose of a danger response. On the other hand, UVR causes immunosuppression via regulatory T cells (Treg) that limit the inflammatory reaction. The concurrent induction of antimicrobial peptides and Treg by UVR may represent a counter-regulatory mechanism in response to barrier disruption, preventing microbial superinfection and sensitization to contact allergens, respectively, both of which cross impaired epidermis more easily. Thus, using a model of murine contact hypersensitivity we examined if disruption of the epidermal barrier only initiates similar counter-regulatory mechanisms via the generation of Treg. Sensitization through tape-stripped skin induced a weaker contact hypersensitivity response than in control mice. This was due to the induction of antigen-specific Treg, as demonstrated in adoptive transfer and depletion experiments utilizing DEREG mice. Treg induction by tape stripping was linked to the expression of the alarmin IL-33, as blockade of IL-33 exacerbated contact hypersensitivity, whereas injection of IL-33 inhibited contact hypersensitivity and induced Treg. These results demonstrate that epidermal barrier disruption, in addition to danger signals, induces regulatory events that prevent exaggerated skin inflammation and that IL-33 appears to be critically involved in this process. |
