Inflammatory cells in renal allografts.
Renal transplants are injured by a variety of diseases and pathways. One important cause for acute and chronic graft failure is rejection. Since the advent of kidney transplantation, it has become apparent that rejection is a cellular and/or antibody mediated inflammatory process with different histologic phenotypes, and clinical degrees of severity. In recent years, the immunohistochemical detection of the complement degradation product C4d has further helped to unravel mechanisms of graft injury. Our brief review of 'renal allograft inflammation' focuses on basic morphologic aspects of rejection. Our goal is to foster the close correlation between 'histologic variants of rejection/inflammation' and molecular signaling cascades including chemokine induced effects.
University of North Carolina Medical School, Department of Pathology and Laboratory Medicine, Chapel Hill, NC 27599-7525, USA. volker_nickeleit@med.unc.edu
Volker
V
Nickeleit
Kenneth
K
Andreoni
D002196:Capillaries / Q000473:pathology; D006084:Graft Rejection / Q000473:pathology; D006644:Histiocytes / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology; D016030:Kidney Transplantation / Q000276:immunology / Q000473:pathology / Q000502:physiology*; D007684:Kidney Tubules / Q000473:pathology / Q000503:physiopathology; D008214:Lymphocytes / Q000502:physiology; D008264:Macrophages / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D009000:Monocytes / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D012077:Renal Artery / Q000473:pathology