| First Author | Yang Y | Year | 2019 |
| Journal | J Dermatol Sci | Volume | 94 |
| Issue | 2 | Pages | 290-297 |
| PubMed ID | 31118160 | Mgi Jnum | J:289648 |
| Mgi Id | MGI:6434567 | Doi | 10.1016/j.jdermsci.2019.04.008 |
| Citation | Yang Y, et al. (2019) Keratinocyte-derived TGFbeta is not required to maintain skin immune homeostasis. J Dermatol Sci 94(2):290-297 |
| abstractText | BACKGROUND: Transforming growth factor beta 1 (TGFbeta) is known to be a regulator of autoimmunity. Loss of TGFbeta leads to severe multi-organ autoimmunity in mice. In skin, role of TGFbeta in suppressing autoimmunity is unclear. OBJECTIVE: Determine whether Keratinocyte (KC)-derived TGFbeta is required for skin immune homeostasis. METHODS: We generated K14-CreER(T2)TGFbeta1(fl/fl) (TGFbeta(DeltaKC)) mice allowing for tamoxifen-induced deletion of TGFbeta1 in KC. The phenotype of skin was analyzed and compared to mice in which epidermal activation of TGFbeta is impaired. RESULTS: KC was the major source of TGFbeta in epidermis. Topical tamoxifen application led to efficient TGFbeta1 deletion. The expected acanthosis was observed but no inflammatory infiltrate or altered numbers of resident immune cells were evident. Similarly, Itgb6(-/-)x K14Cre Itgb8(f/f) (Itgb6(-/-)Itgb8(DeltaKC)) mice lacking both epidermal TGFbeta-activating integrins showed no evidence of cutaneous inflammation. CONCLUSIONS: KC-derived TGFbeta and epidermal TGFbeta activation are not required to suppress skin autoimmunity in steady state. |
