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Innate immunity in heart transplantation
Timothy M Millington1, Joren C Madsen
1Massachusetts General Hospital, Boston, Massachusetts, USA.
Insights
The innate immune system plays a key role in cardiac allograft vasculopathy (CAV) after heart transplants. Targeting innate immunity may prevent CAV and improve graft tolerance.
Area of Science:
- Immunology
- Transplantation Medicine
- Cardiology
Background:
- Cardiac transplantation is the primary treatment for end-stage heart failure.
- Cardiac allograft vasculopathy (CAV) limits transplant efficacy.
- Conventional immunosuppression inadequately targets the innate immune system.
Purpose of the Study:
- To review the role of the innate immune system in cardiac allograft rejection and CAV.
- To highlight the contribution of innate immune responses to adaptive immunity and CAV development.
Main Methods:
- Review of current literature on innate immunity in cardiac transplantation.
- Analysis of the roles of Toll-like receptors, natural killer cells, and complement in rejection.
- Examination of mechanisms linking innate immunity to CAV.
Main Results:
- Innate immune activation via Toll-like receptors contributes to an inflammatory environment promoting rejection.
- Natural killer cells possess memory-like properties and play an underestimated role in cardiac allograft rejection.
- Complement deposition is implicated in acute cellular rejection and the development of CAV.
Conclusions:
- The innate immune system is a critical, yet often overlooked, factor in allograft rejection.
- Targeting Toll-like receptors, natural killer cells, and complement presents a promising strategy for preventing CAV.
- Modulating innate immunity may be key to achieving long-term tolerance in cardiac allografts.
Purpose Of Review:
Cardiac transplantation is the treatment of choice for end-stage heart failure, but its efficacy is limited by the development of cardiac allograft vasculopathy (CAV). Although the adaptive immune system is efficiently suppressed by conventional drugs, the innate immune system is largely unaffected. The innate response may contribute both to stimulation of the adaptive response and to the future development of CAV.
Recent Findings:
Stimulation of Toll-like receptors by endogenous ligands released in response to ischemia/reperfusion causes an inflammatory milieu favorable to graft rejection and unfavorable to tolerance. New evidence suggests that natural killer cells have previously unknown memory-like features and are capable of graft rejection. Their role in rejecting the cardiac allograft has previously been underestimated. Complement deposition may also contribute to acute cellular rejection and CAV.
Summary:
The innate immune system is an important but neglected component of allograft rejection. Drugs that target Toll-like receptors, natural killer cells and complement may play an important role in preventing CAV and achieving tolerance to cardiac allografts.
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