Current trends in transplant immunology

Current Opinion in Nephrology and Hypertension

Volumn 8, Issue 3, 1999, Pages 317-324

  Hancock, Wayne W ^a,b  

^a MILLENNIUM PHARMACEUTICALS INC   (United States)

^b HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

INTERLEUKIN 2 RECEPTOR ANTIBODY; MONOCLONAL ANTIBODY; MONOCLONCAL ANTIBODY CD40L; UNCLASSIFIED DRUG;

ALLOIMMUNITY; APOPTOSIS; BLOOD CLOTTING; BRAIN DEATH; GENE ACTIVITY; GRAFT PRESERVATION; GRAFT REJECTION; HISTOCOMPATIBILITY; HUMAN; IMMUNE RESPONSE; IMMUNOBIOLOGY; IMMUNOLOGICAL TOLERANCE; IMMUNOPATHOGENESIS; KIDNEY ALLOGRAFT REJECTION; KIDNEY DONOR; KIDNEY ISCHEMIA; KIDNEY PERFUSION; KIDNEY TRANSPLANTATION; NONHUMAN; PRIORITY JOURNAL; REPERFUSION INJURY; REVIEW; XENOTRANSPLANTATION;

ANIMALS; APOPTOSIS; BRAIN DEATH; HUMANS; IMMUNOSUPPRESSION; ISOANTIGENS; KIDNEY; KIDNEY TRANSPLANTATION; REPERFUSION INJURY; TISSUE DONORS; TRANSPLANTATION, HETEROLOGOUS;

EID: 0032799836     PISSN: 10624821     EISSN: None     Source Type: Journal    
DOI: 10.1097/00041552-199905000-00007     Document Type: Review

References (74)

1. Takada M, Nadeau KC, Hancock WW, Mackenzie HS, Shaw GD, Waaga AM, et al. Effects of explosive brain death on cytokine activation of peripheral organs in the rat. Transplantation 1998; 65:1533-1542. This study demonstrates the deleterious effects of brain death on peripheral organs used for transplantation, including the kidney, as a result of the release of soluble mediators; effects on peripheral organs were significantly decreased by therapy with recombinant proteins which inhibit P- and E-selectin binding or CD28:B7 interactions.
2. Pratschke J, Kusaka M, Wilhem MJ, Hancock WW, Tilney NL. Accelerated rate of acute rejection of renal allografts from brain dead donors. Surg Forum 1998;69:364-366. Along with Reference [1], this study indicates that brain death can damage kidneys and increases the severity of acute rejection after their transplantation.
3. Frasca L, Amendola A, Hornick P, Brookes P, Aichinger G, Marelli-Berg F, et al. Role of donor and recipient antigen-presenting cells in priming and maintaining T cells with indirect allospecificity. Transplantation 1998; 66:1238-1243.
4. Deckers JG, Daha MR, Van der Kooij SW, Van der Woude FJ. Epithelial- and endothelial-cell specificity of renal graft infiltrating T cells. Clin Transplant 1998; 12:285-291.
5. Kwon O, Nelson WJ, Sibley R, Huie P, Scandling JD, Dafoe D, et al. Backleak, tight junctions, and cell-cell adhesion in postischemic injury to the renal allograft. J Clin Invest 1998; 101:2054-2064. An interesting paper which demonstrates backleak across tubules as a key mechanism in clinical ischemia/reperfusion injury.
6. Sims TN, Goes NB, Ramassar V, Urmson J, Halloran PF. In vivo class II transactivator expression in mice is induced by a non-interferon-gamma mechanism in response to local injury. Transplantation 1997; 64:1657-1664. Class II induction has long been regarded as a key IFN-γ-dependent event. This paper shows that class II-induction can also occur in IFN-γ knockout mice.
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15. Brenner BM, Mackenzie HS. Nephron mass as a risk factor for progression of renal disease. Kidney Int 1997; 63 (Suppl):S124-127. An interesting discussion of the role of nephron mass in chronic renal injury, with sobering implications for the use of pediatric kidneys for organ donation.
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29. Sharma VK, Bologa RM, Li BG, Xu GP, Lagman M, Hiscock W, et al. Molecular executors of cell death differential intrarenal expression of Fas ligand, Fas, granzyme B, and perforin during acute and/or chronic rejection of human renal allografts. Transplantation 1996; 62:1860-1866.
30. Tang WH, Friess H, di Mola FF, Schilling M, Maurer C, Graber HU, et al. Activation of the serine proteinase system in chronic kidney rejection. Transplantation 1998; 65:1628-1634.
31. Hancock Buelow R, Sayegh MH, Turka LA. Antibody-induced transplant arteriosclerosis is prevented by graft expression of anti-oxidant and anti-apoptotic genes. Nature Med 1998; 4:1392-1396. This paper reviews data concerning the role of anti-apoptotic genes, which also effectively suppress the activation of NFκB in endothelial and smooth muscle cells, in the maintenance of tolerance in experimental cardiac allografts and xenografts.
32. Hancock WW, Tran TH, Kao J. Induction of protective gene expression within graft endothelial cells as a means to control NFκB activation and development of chronic rejection. Graft 1998; 1 (Suppl. II):21-24. This study documents the in-vitro and in-vivo effects of engineering high-level endothelial protective gene expression and tetracycline-dependent inducible inhibition of NFκB.
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