Regulatory T cells are required for normal and activin-promoted wound repair in mice

Abstract

Healing of skin wounds is orchestrated by various types of immune cells, but little is known about the role of FoxP3⁺ regulatory T cells (Tregs) in this process. Here we determined if Tregs are important for wound healing in normal mice and if they contribute to the accelerated healing of mice overexpressing the growth and differentiation factor activin. Diphtheria-toxin induced Treg depletion prior to injury caused impaired healing characterized by delayed re-epithelialization, reduced wound contraction and impaired vessel maturation. The accelerated wound repair of activin-transgenic mice was also abrogated. Mechanistically, we found a strong increase in IL-4 levels combined with overrepresentation of T-bet⁺ and GATA-3⁺ αβ T cells in Treg-depleted 7-day wounds. In addition, numbers of IFNγ- or IL-17A-producing CD4⁺ and CD4⁻ T cells were elevated. These results demonstrate that Treg depletion in wounds facilitates the expansion of an αβ T cell population with features of Th1 and Th2 cells, and suggest that concomitant changes in the cytokine milieu disturb the healing process.

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