[Frontiers in Bioscience E1, 600-604, June 1, 2009]

Toll-like receptors, innate immunity and lung transplantation

Laurie D. Snyder1, Scott M. Palmer2

1Department of Medicine, Duke University Medical Center, Box 102043,Durham, NC 27710, 2 Department of Medicine, Duke University Medical Center, Box 3876, Durham, NC 27710

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Toll-like Receptors
4. Collectins
5. Defensins
6. Complement
7. Summary
8. Acknowledgement
9. References

1. ABSTRACT

Lung transplant allografts have the highest rate of rejection and shortest graft survival time among the commonly transplanted solid organs despite high levels of immunosuppression. This observation strongly indicates that mechanisms unique to the lung allograft contribute to rejection post lung transplant. Unlike most other solid organ recipients, the lung allograft is exposed to both the external environment and a significant amount of donor-derived lymphatic and structural tissue. For these reasons, the recipient's innate immune system may be critically involved in the initiation and maintenance of rejection after lung transplant. The strongest evidence for innate immune activation participating in lung allograft rejection is based upon genetic studies which demonstrate that variation in toll-like receptors and the related molecule CD14 modulate posttransplant lung allograft rejection. However, secreted pathogen recognition receptors, including defensins and collectins, and complement are parts of the innate pulmonary host defense and may be important in lung transplant rejection. This report will review the current understanding of innate immunity in lung allograft rejection in both murine and human studies.