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Depletion of langerin+ cells enhances cutaneous wound healing

descriptionPublicationkeyboard_double_arrow_right Article 15 May 2020 English Publisher:WileyJournal:Immunology, volume 160, pages 366-381 (issn: 0019-2805, eissn: 1365-2567,

Authors: Aarthi Rajesh; Gabriella Stuart; Nicola Real; Jenny Ahn; Allison Tschirley; Lyn Wise; Merilyn Hibma;

doi: 10.1111/imm.13202

pmid: 32307696

pmc: PMC7370135

Depletion of langerin+ cells enhances cutaneous wound healing

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Abstract

SummaryLangerin is a C‐type lectin receptor that is expressed on Langerhans cells and langerin‐positive dermal dendritic cells in the skin. Little is known about the function of langerin+ cells in wound healing. In this study, the effects of ablation of langerin+ cells on healing of a full‐thickness excision wound were investigated using the langerin‐DTR depletable mouse. Strikingly, depletion of langerin+ cells resulted in more rapid reduction in wound area. Accelerated wound healing in the langerin+‐cell‐depleted group was characterized by enhanced neo‐epidermis and granulation tissue formation, and increased cellular proliferation within the newly formed tissues. Accelerated healing in the absence of langerin+ cells was associated with increased levels of granulocyte–macrophage colony‐stimulating factor, F4/80+ cells and blood vessels within the granulation tissue. These data support an inhibitory role for langerin+ cells during wound healing. Therapies that suppress langerin+ cells or their function may therefore have utility in progressing the healing of wounds in humans.

Related Organizations

University of Otago
New Zealand

Keywords

Mice, Knockout, Wound Healing, Granulocyte-Macrophage Colony-Stimulating Factor, Dendritic Cells, Mice, Inbred C57BL, Mice, Mannose-Binding Lectins, Langerhans Cells, Antigens, Surface, Granulation Tissue, Animals, Angiogenesis Inducing Agents, Female, Lectins, C-Type, Cells, Cultured, Cell Proliferation, Skin

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	impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.	Top 10%