Background
Transforming growth factor beta 1 (TGFβ) is known to be a regulator of autoimmunity. Loss of TGFβ leads to severe multi-organ autoimmunity in mice. In skin, role of TGFβ in suppressing autoimmunity is unclear.
Conclusions
KC-derived TGFβ and epidermal TGFβ activation are not required to suppress skin autoimmunity in steady state.
Methods
We generated K14-CreERT2TGFβ1fl/fl (TGFβΔKC) mice allowing for tamoxifen-induced deletion of TGFβ1 in KC. The phenotype of skin was analyzed and compared to mice in which epidermal activation of TGFβ is impaired.
Objective
Determine whether Keratinocyte (KC)-derived TGFβ is required for skin immune homeostasis.
Results
KC was the major source of TGFβ in epidermis. Topical tamoxifen application led to efficient TGFβ1 deletion. The expected acanthosis was observed but no inflammatory infiltrate or altered numbers of resident immune cells were evident. Similarly, Itgb6-/-x K14Cre Itgb8f/f (Itgb6-/-Itgb8ΔKC) mice lacking both epidermal TGFβ-activating integrins showed no evidence of cutaneous inflammation. Conclusions: KC-derived TGFβ and epidermal TGFβ activation are not required to suppress skin autoimmunity in steady state.