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Human CD31 on Swine Endothelial Cells Induces SHP-1 Phosphorylation in Macrophages
- Source :
- Transplantation proceedings. 52(6)
- Publication Year :
- 2019
-
Abstract
- Background Innate immunity by natural killer (NK) cells, macrophages, and neutrophils cause severe rejections in xenotransplantation. Therefore, the development of strategies for suppressing macrophages has considerable potential in practical applications of xenotransplantation. Recently, we found that human CD31 on swine endothelial cells (SECs) suppresses neutrophil-mediated xenogeneic rejection through homophilic binding. Since a significant amount of CD31 is expressed not only on neutrophils but also on macrophages, we studied the function of human CD31 in macrophage-mediated cytotoxicity. Methods SECs and hCD31-transfected SECs (SEC/hCD31) were co-cultured with macrophages and cytotoxicity by macrophages was evaluated with water-soluble tetrazolium salt, or WST-8, assay. To confirm whether or not inhibitory signals are induced by hCD31 homophilic binding, the phosphorylation of the enzyme SHP-1 was investigated with Western blotting. Results No suppression of cytotoxicity was induced in macrophages that had been co-cultured with SEC/CD31. However, phosphorylation of SHP-1 was induced in macrophages that had been co-cultured with SEC/hCD31. Conclusions Human CD31 on SEC may induce not only inhibitory signals but also activation signals via the binding to other receptors for hCD31.
- Subjects :
- CD31
Cytotoxicity, Immunologic
Graft Rejection
Swine
Xenotransplantation
medicine.medical_treatment
Transfection
medicine
Animals
Humans
Phosphorylation
Receptor
Cytotoxicity
Transplantation
Innate immune system
Chemistry
Macrophages
Protein Tyrosine Phosphatase, Non-Receptor Type 6
Endothelial Cells
Coculture Techniques
Cell biology
Blot
Platelet Endothelial Cell Adhesion Molecule-1
Heterografts
Surgery
Subjects
Details
- ISSN :
- 18732623
- Volume :
- 52
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- Transplantation proceedings
- Accession number :
- edsair.doi.dedup.....5cb1b2f3d50aff5bada92b4ac4042828