title: Monocytes/macrophages in kidney allograft intimal arteritis: no association with markers of humoral rejection or with inferior outcome.
abstract: BACKGROUND
  Several studies indicate that interstitial and intracapillary monocytes/macrophages (MO) represent a significant proportion of graft-infiltrating cells in renal allografts and that their presence may unfavourably affect clinical outcome. Much less is known about the role of MO in vascular rejection of transplanted kidneys. The aim of our study was to determine the cellular composition of immune cell infiltrates in intimal arteritis and to analyse whether it is associated with features of humoral immunity and impaired graft survival.
  
  
  METHODS
  In 34 recipients with vascular rejection, we determined the proportion of intimal and interstitial MO and T-cells (expressed as ratio of CD68- and CD3-positive cells) in immunohistochemically double-labelled slides.
  
  
  RESULTS
  Intimal arteritis is always composed of T-cells and MO with a median CD68/CD3 ratio of 1.03. In 47% of cases, however, T-cells predominate (CD68/CD3 ratio <1). The median interstitial CD68/CD3 ratio is 0.61, with T-cells dominating in 64% of cases. There is no correlation between the cellular composition of arterial and interstitial infiltrates. The proportion of interstitial and arterial MO has no impact on graft survival, and is, in contrast to previous reports on MO in allograft glomerulitis and capillaritis, not associated with C4d staining.
  
  
  CONCLUSIONS
  Intimal arteritis in kidney allograft rejection is composed of a mixed infiltrate of MO and T-lymphocytes. In contrast to MO in PTCitis and glomerulitis, the MO in intimal arteritis are not associated with markers of humoral immune response and there are no different allograft outcomes between MO and T-lymphocyte-dominated groups.
authors.affiliation: Clinical Institute of Pathology, Medical University of Vienna, Währinger Gürtel 18-20, A-1090, Vienna, Austria.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Kozakowski
authors.forename: Georg A
authors.initials: GA
authors.lastname: Böhmig
authors.forename: Markus
authors.initials: M
authors.lastname: Exner
authors.forename: Afschin
authors.initials: A
authors.lastname: Soleiman
authors.forename: Nicole
authors.initials: N
authors.lastname: Huttary
authors.forename: Katalin
authors.initials: K
authors.lastname: Nagy-Bojarszky
authors.forename: Rupert C
authors.initials: RC
authors.lastname: Ecker
authors.forename: Zeljko
authors.initials: Z
authors.lastname: Kikić
authors.forename: Heinz
authors.initials: H
authors.lastname: Regele
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001167:Arteritis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D017252:CD3 Complex / Q000378:metabolism; D005260:Female; D006084:Graft Rejection / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D006801:Humans; D053208:Kaplan-Meier Estimate; D016030:Kidney Transplantation / Q000009:adverse effects* / Q000276:immunology / Q000473:pathology; D008264:Macrophages / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D014184:Transplantation, Homologous; D016896:Treatment Outcome; D017539:Tunica Intima / Q000276:immunology / Q000473:pathology; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; C067980:CD68 antigen, human; D000097382:CD68 Molecule