GARP Regulates the Immune Capacity of a Human Autologous Platelet Concentrate

Autologous platelet concentrates, like liquid platelet rich fibrin (iPRF), optimize wound healing; however, the underlying immunological mechanisms are poorly understood. Platelets, the main cellular component of iPRF, highly express the protein, Glycoprotein A repetitions predominant (GARP), on the...

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Bibliographic Details
Published in:Biomedicines 2022-12, Vol.10 (12), p.3136
Main Authors: Trzeciak, Emily R, Zimmer, Niklas, Kämmerer, Peer W, Thiem, Daniel, Al-Nawas, Bilal, Tuettenberg, Andrea, Blatt, Sebastian
Format: Article
Language:English
Subjects:
Angiogenesis
Anticoagulants
autologous platelet concentrate
Blood platelets
CD4 antigen
Fibrin
Foxp3 protein
GARP
Genotype & phenotype
Growth factors
Health aspects
Immunological tolerance
Influence
Interleukin 2
iPRF
liquid platelet rich fibrin
Lymphocytes
Lymphocytes T
Macrophages
Monocytes
Phenotypes
Platelets
TGF-ß
Tissue engineering
Wound healing
γ-Interferon
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Summary:Autologous platelet concentrates, like liquid platelet rich fibrin (iPRF), optimize wound healing; however, the underlying immunological mechanisms are poorly understood. Platelets, the main cellular component of iPRF, highly express the protein, Glycoprotein A repetitions predominant (GARP), on their surfaces. GARP plays a crucial role in maintaining peripheral tolerance, but its influence on the immune capacity of iPRF remains unclear. This study analyzed the interaction of iPRF with immune cells implicated in the wound healing process (human monocyte derived macrophages and CD4 T cells) and evaluated the distinct influence of GARP on these mechanisms in vitro. GARP was determined to be expressed on the surface of platelets and to exist as a soluble factor in iPRF. Platelets derived from iPRF and iPRF itself induced a regulatory phenotype in CD4 T cells, shown by increased expression of Foxp3 and GARP as well as decreased production of IL-2 and IFN-γ. Application of an anti-GARP antibody reversed these effects. Additionally, iPRF polarized macrophages to a "M0/M2-like" phenotype in a GARP independent manner. Altogether, this study demonstrated for the first time that the immune capacity of iPRF is mediated in part by GARP and its ability to induce regulatory CD4 T cells.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines10123136