Highlights
- •K14-CreERT2 TGFβ1fl/fl mice develop acanthosis.
- •K14-CreERT2 TGFβ1fl/fl mice do not develop spontaneous skin inflammation.
- •Itgb6−/− x K14Cre Itgb8f/f mice do not develop spontaneous skin inflammation.
Abstract
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.
Objective
Determine whether Keratinocyte (KC)-derived TGFβ is required for skin immune homeostasis.
Methods
We generated K14-CreERT2 TGFβ1fl/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.
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.
Keywords
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Article info
Publication history
Published online: May 07, 2019
Accepted:
April 25,
2019
Received in revised form:
April 24,
2019
Received:
April 9,
2019
Identification
Copyright
© 2019 Japanese Society for Investigative Dermatology. Published by Elsevier B.V. All rights reserved.
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- Corrigendum to “Keratinocyte-derived TGFβ is not required to maintain skin immune homeostasis” [J. Dermatol. Sci. 94 (2) (2019) 290–297]Journal of Dermatological ScienceVol. 95Issue 3