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Mouse Kidney Transplantation: Models of Allograft Rejection
Published on: October 11, 2014
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Chronic allograft rejection: a fresh look.
Johannes Wedel1, Sarah Bruneau, Nora Kochupurakkal
1aTransplant Research Program, Pediatric Transplant Center bDepartment of Medicine, Division of Nephrology, Boston Children's Hospital cDepartment of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
Current Opinion in Organ Transplantation
|January 8, 2015
Summary
Graft microenvironment molecules influence chronic rejection. Targeting mTOR/Akt signaling and semaphorin-neuropilin pathways may enhance immunoregulation and long-term graft survival.
Area of Science:
- Transplantation immunology
- Molecular biology
- Immunoregulation
Background:
- Chronic rejection is influenced by graft microenvironment factors.
- Ischemia-reperfusion injury triggers inflammatory responses within the graft.
Purpose of the Study:
- To review new developments in understanding chronic rejection.
- To explore molecular mechanisms dictating graft rejection phenotype and evolution.
Main Methods:
- Review of current literature on graft rejection.
- Analysis of molecular signaling pathways involved in immune responses.
Main Results:
- Hypoxia-inducible factor 1α drives pro-inflammatory factor expression post-injury.
- Vascular endothelial growth factor (VEGF) recruits allogeneic T cells.
- mTOR/Akt signaling promotes pro-inflammatory phenotypes; inhibition induces anti-inflammatory and immunoregulation.
- Semaphorin-neuropilin interactions may stabilize regulatory T cell function and inhibit Akt-induced responses.
Conclusions:
- mTOR/Akt signaling within the graft promotes chronic rejection.
- Semaphorin-neuropilin biology offers a novel therapeutic target for enhancing graft survival.
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