Journal
TRANSPLANTATION PROCEEDINGS
Volume 45, Issue 6, Pages 2513-2516Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.transproceed.2013.02.126
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Background. NKG2D (natural killer group 2 member D), are activating or coactivating receptor on NK cells, gamma delta T, and CD8(+) T cells, stimulates cytokine secretion by the former two and plays a costimulatory role for the last CD8(+) T cells. Methods. Male Lewis rat hearts were flushed and stored in cold Bretschneider preservation solution for 8 hours. Anti-NKG2D monoclonal antibody (mAb) was administered before transplantation into syngeneic recipients. Expressions of Troponin-T, myeloperoxidase (MPO), tumor necrosis factor (INF), (ICAM) and interleukin (IL)-17 were examined on days 1, 3, and 7 after reperfusion. Results. We observed that isografts from anti-NKG2D mAb-treated animals showed decreased cardiac troponin-T, low expression of MPO, TNF, and ICAM, and superior cardiac output. Furthermore, blockade of NKG2D significantly reduced the number of gamma delta T cells, which are the main source of IL-17 production. Conclusion. Blockade of NKG2D significantly attenuated ischemia-reperfusion injury in a cardiac transplantation model. The effect coincided with a low expression of TNF alpha, ICAM and a reduced number of infiltrating IL-17-producing gamma delta T cells.
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