title: The cellular lesion of humoral rejection: predominant recruitment of monocytes to peritubular and glomerular capillaries.
abstract: Accumulation of inflammatory cells within capillaries is a common morphologic feature of humoral renal allograft rejection and is most easily appreciated if it occurs in glomeruli. The aim of our study was to determine the amount and composition of immune cells within glomeruli and peritubular capillaries (PTC) in cellular and humoral allograft rejection. Immunofluorescent double-labeling for CD31 and CD3 or CD68 was used for phenotyping and enumerating immune cells within glomeruli and PTC. The major findings are: (1) accumulation of immune cells in PTC is far more common than it would be anticipated based on the assessment by conventional histology; (2) it is not the absolute number of immune cells accumulating within capillaries, but rather the composition of the intracapillary cell population that distinguishes humoral rejection from cellular rejection and (3) in C4d positive biopsies a predominantly monocytic cell population accumulates not only within glomeruli but also within PTC. The median value of monocyte/T-cell ratio within PTC was 2.3 in C4d positive biopsies but only 1 (p = 0.0008) in C4d negative biopsies. Given their prominent presence within capillaries and their extensive biological versatility monocytes might contribute to the capillary damage observed in acute and chronic allograft rejection.
authors.affiliation: Clinical Institute of Pathology, Medical University of Vienna, Vienna, Austria.
authors.forename: T
authors.initials: T
authors.lastname: Fahim
authors.forename: G A
authors.initials: GA
authors.lastname: Böhmig
authors.forename: M
authors.initials: M
authors.lastname: Exner
authors.forename: N
authors.initials: N
authors.lastname: Huttary
authors.forename: H
authors.initials: H
authors.lastname: Kerschner
authors.forename: S
authors.initials: S
authors.lastname: Kandutsch
authors.forename: D
authors.initials: D
authors.lastname: Kerjaschki
authors.forename: A
authors.initials: A
authors.lastname: Bramböck
authors.forename: K
authors.initials: K
authors.lastname: Nagy-Bojarszky
authors.forename: H
authors.initials: H
authors.lastname: Regele
mesh_terms: D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001706:Biopsy; D017252:CD3 Complex / Q000378:metabolism; D002196:Capillaries / Q000473:pathology*; D015935:Complement C4b / Q000378:metabolism; D006084:Graft Rejection / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007678:Kidney Glomerulus / Q000098:blood supply*; D016030:Kidney Transplantation / Q000276:immunology* / Q000473:pathology; D007684:Kidney Tubules / Q000098:blood supply*; D009000:Monocytes / Q000276:immunology / Q000473:pathology*; D009504:Neutrophils / Q000276:immunology / Q000473:pathology; D010446:Peptide Fragments / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D012189:Retrospective Studies; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D014184:Transplantation, Homologous / Q000276:immunology / Q000473:pathology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D015935:Complement C4b; D010446:Peptide Fragments; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C032261:complement C4d