title: NKG2D blockade significantly attenuates ischemia-reperfusion injury in a cardiac transplantation model.
abstract: BACKGROUND
  NKG2D (natural killer group 2 member D), are activating or coactivating receptor on NK cells, γδ 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 γδ T cells, which are the main source of IL-17 production.
  
  
  CONCLUSIONS
  Blockade of NKG2D significantly attenuated ischemia-reperfusion injury in a cardiac transplantation model. The effect coincided with a low expression of TNFα, ICAM and a reduced number of infiltrating IL-17-producing γδ T cells.
authors: Department of Cardiology, Renmin Hospital of Wuhan University, People's Republic of China.
authors: B
authors: B
authors: Shen
authors: J
authors: J
authors: Li
authors: B
authors: B
authors: Yang
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D050377:Cold Ischemia / Q000009:adverse effects; D019610:Cytoprotection; D004195:Disease Models, Animal; D005947:Glucose / Q000633:toxicity; D016027:Heart Transplantation / Q000009:adverse effects*; D006439:Hemodynamics / Q000187:drug effects; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D037181:Lectins, C-Type / Q000037:antagonists & inhibitors* / Q000378:metabolism; D008297:Male; D008353:Mannitol / Q000633:toxicity; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000276:immunology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D055655:NK Cell Lectin-Like Receptor Subfamily K / Q000037:antagonists & inhibitors* / Q000378:metabolism; D019188:Organ Preservation Solutions / Q000633:toxicity; D009195:Peroxidase / Q000378:metabolism; D011189:Potassium Chloride / Q000633:toxicity; D011343:Procaine / Q000633:toxicity; D051381:Rats; D011917:Rats, Inbred Lew; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism; D020127:Recovery of Function; D013997:Time Factors; D020107:Troponin T / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; C039984:Bretschneider cardioplegic solution; D020381:Interleukin-17; D037181:Lectins, C-Type; D055655:NK Cell Lectin-Like Receptor Subfamily K; C113208:NKR-P2 protein, rat; D019188:Organ Preservation Solutions; D016692:Receptors, Antigen, T-Cell, gamma-delta; D020107:Troponin T; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008353:Mannitol; D011343:Procaine; D011189:Potassium Chloride; D009195:Peroxidase; D005947:Glucose