title: Quilty effect areas are frequently associated with endocardial C4d deposition.
abstract: BACKGROUND
  The meaning and clinical implications of the Quilty effect (QE) are not entirely clear. In some biopsies we have found complement split C4d deposition in QE areas, but we do fully comprehend the frequency or pathogenic relationships involved. The objective of this study was to gain insight into the immunologic events involved in the QE, and to understand if and how it relates to complement activation.
  
  
  METHODS
  Protocol allograft biopsies (January to December 2005) with evidence of the QE, without cellular rejection or changes suspicious for antibody-mediated rejection, were selected for C4d, CD3, CD20 and CD68 immunohistochemistry.
  
  
  RESULTS
  Among 128 allograft biopsies (42 patients), 17 (11 patients) fulfilled the inclusion criteria. Eleven of the 17 biopsies (64.7%), from 8 patients, showed C4d deposition in the endocardium; the positivity was interestingly linear in the endocardium and surrounded by the lymphocytes forming the Quilty lesion. In some cases, the linear C4d deposition extended to the endocardium surrounding the QE area. This pattern was not detected in any of 66 heart allograft biopsies without the QE. B cells were second to T cells in their contribution to the QE, comprising a median of 40% (range, 20% to 50%) of the cells. C4d deposition was not associated with clinical alterations.
  
  
  CONCLUSIONS
  The QE is frequently associated with C4d deposition in the endocardium of patients without evidence of rejection. This event suggests a pathogenic relationship between the QE and complement activation. It is possible that the simultaneous presence of both features in an allograft heart biopsy, without evidence of rejection, indicates better adaptation of allograft to host ("accommodation"); however, the precise meaning and implications are not yet known.
authors.affiliation: Department of Pathology, Faculty of Medicine, University of Antioquia, Medellín, Colombia.
authors.forename: Luis C
authors.initials: LC
authors.lastname: Cano
authors.forename: Ariel A
authors.initials: AA
authors.lastname: Arteta
authors.forename: Ricardo
authors.initials: R
authors.lastname: Fernández
authors.forename: José A Lopez
authors.initials: JA
authors.lastname: García-Asenjo
authors.forename: Susana
authors.initials: S
authors.lastname: Hernández
authors.forename: Darío
authors.initials: D
authors.lastname: Fernández
authors.forename: Luis F
authors.initials: LF
authors.lastname: Arias
mesh_terms: D015703:Antigens, CD; D018951:Antigens, CD20; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex / Q000032:analysis; D015935:Complement C4b / Q000032:analysis*; D004699:Endocardium / Q000276:immunology* / Q000473:pathology; D005260:Female; D006084:Graft Rejection / Q000276:immunology* / Q000473:pathology; D016027:Heart Transplantation / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007120:Immunochemistry; D008297:Male; D009206:Myocardium / Q000276:immunology* / Q000473:pathology; D010446:Peptide Fragments / Q000032:analysis*; D012189:Retrospective Studies; D014184:Transplantation, Homologous; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D018951:Antigens, CD20; D015214:Antigens, Differentiation, Myelomonocytic; D017252:CD3 Complex; D015935:Complement C4b; D010446:Peptide Fragments; C067980:CD68 antigen, human; D000097382:CD68 Molecule; C032261:complement C4d