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Abstract
Regulatory T cells (Tregs) suppress immune responses and maintain immunological self-tolerance and homeostasis. We currently investigated relationships between skin barrier condition and Treg behavior using skin barrier-disrupted mice. Skin barrier disruption was induced by repeated topical application of 4% sodium dodecyl sulfate (SDS) on mice. The number of CD4+ forkhead box protein P3 (Foxp3)+ Tregs was higher in 4% SDS-treated skins than in controls. This increasing was correlated with the degree of acanthosis. The numbers of interleukin (IL)-10+ and transforming growth factor (TGF)-β+ Tregs also increased in 4% SDS-treated skins. Localization of IL-33 in keratinocytes shifted from nucleus to cytoplasm after skin barrier disruption. Notably, IL-33 promoted the migration of Tregs in chemotaxis assay. The skin infiltration of Tregs was cancelled in IL-33 neutralizing antibody-treated mice and IL-33 knockout mice. Thus, keratinocyte-derived IL-33 may induce Treg migration into barrier-disrupted skin to control the phase transition between healthy and inflammatory conditions.
Highlights
The skin is an important barrier that protects against invasion by foreign substances, including harmful microorganisms and irritants, and retains water in the body [1,2]
Erythema and/or dryness were slight by 4% sodium dodecyl sulfate (SDS) application (Figure 1a), the Erythema and/or dryness were slight by 4% SDS application (Figure 1a), the dermatitis score in 4% SDS-treated mice on days 11 to 18 was significantly higher than that dermatitis score in 4% SDS-treated mice on days 11 to 18 was significantly higher than in naïve or vehicle-treated mice (Figure 1b)
We used a mouse model of skin barrier disruption, which was induced by the repeated application of the surfactant SDS
Summary
The skin is an important barrier that protects against invasion by foreign substances, including harmful microorganisms and irritants, and retains water in the body [1,2]. Occurring CD25+ CD4+ Tregs, which express the transcription factor forkhead box protein P3 (Foxp3) [5,6,7,8], actively maintain immunological self-tolerance and homeostasis through the secretion of cytokines such as interleukin (IL)-10 and transforming growth factor (TGF)-β [9,10]. The fatal multiorgan autoinflammatory destruction in both immune dysregulation, polyendocrinopathy, enteropathy, and X-linked syndrome (IPEX) patients and scurfy mice is caused by mutations in the transcriptional regulator Foxp3 [11,12]. Natural mutations in the FOXP3 gene cause the fatal autoimmune Scurfy phenotype in mice and IPEX syndrome in humans [7,13,14,15]
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