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

  • Haertel E Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Switzerland.
  • Joshi N Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Switzerland.
  • Hiebert P Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Switzerland.
  • Kopf M Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Switzerland.
  • Werner S Department of Biology, Institute of Molecular Health Sciences, ETH Zurich, Switzerland.
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  • 2018-02-20
Published in:
  • European journal of immunology. - 2018
Activin
Cytokine
Inflammation
Treg
Wound healing
Activins
Animals
Cell Differentiation
Cell Proliferation
Cells, Cultured
Cytokines
Diphtheria Toxin
Forkhead Transcription Factors
GATA3 Transcription Factor
Mice
Mice, Inbred C57BL
Mice, Transgenic
Promoter Regions, Genetic
T-Box Domain Proteins
T-Lymphocytes, Regulatory
Th1 Cells
Th2 Cells
Wound Healing
English 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 reepithelialization, 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 IFN-γ- 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.
Language
  • English
Open access status
bronze
Identifiers
Persistent URL
https://sonar.rero.ch/global/documents/250363
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