Abstract
Human skin protects the body against infection and injury. This protection involves immune and epithelial cells, but their interactions remain largely unknown. Here, we show that cultured epidermal keratinocytes inhibit allogenic CD4+ T-cell proliferation under both normal and inflammatory conditions. Inhibition occurs through the secretion of soluble factors, including TGFB1 and the cell-surface expression of HLA-G1 and PD-L1 immune checkpoints. For the first time, we here describe the expression of the HLA-G1 protein in healthy human skin and its role in keratinocyte-driven tissue immunomodulation. The overexpression of HLA-G1 with an inducible vector increased the immunosuppressive properties of keratinocytes, opening up perspectives for their use in allogeneic settings for cell therapy.
Highlights
Accepted: 4 June 2021Skin grafting can be necessary in various pathological conditions, such as burns [1], traumatic injury or ulcers (Buruli ulcer, diabetes, pressure, venous ulcer), postoperatively, postinfection, or in genetic diseases such as junctional epidermolysis bullosa [2].Keratinocytes constitute the main cellular component of the epidermis
peripheral blood mononuclear cell (PBMC) activated by CD3+ CD28+ beads were used as positive controls
25,000, 2500, 250 or 0 keratinocytes of one representative donor were incubated with 100,000 PBMCs for 7 days
Summary
Skin grafting can be necessary in various pathological conditions, such as burns [1], traumatic injury or ulcers (Buruli ulcer, diabetes, pressure, venous ulcer), postoperatively, postinfection (necrotizing fasciitis, purpura fulminans), or in genetic diseases such as junctional epidermolysis bullosa [2]. Keratinocytes constitute the main cellular component of the epidermis. The keratinocytes are amplified ex vivo for 1 to. There have been several clinical studies on ex vivo keratinocyte amplification for skin autografts. One reported 65% transplant uptake in 63 burn patients, with 84% patient survival at 7 days [6].
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