title: Interpreting CD56+ and CD163+ infiltrates in early versus late renal transplant biopsies.
abstract: BACKGROUND
  CD56+ and CD163+ cell infiltration in human kidney transplant biopsies have not been fully evaluated.
  
  
  METHODS
  We investigated the association of CD56+ and CD163+ cell infiltration with human kidney transplant biopsies with antibody- or T-cell-mediated rejection (TCMR) and other histologic lesions. One hundred and seventy four clinically indicated transplant biopsies were included in this analysis. Immunohistochemical staining for C4d, CD56 and CD163 was performed.
  
  
  RESULTS
  One hundred and seventy four indication biopsies were divided into early (≤1 year posttransplant; n = 49) and late (>1 year posttransplant; n = 125) biopsies. High numbers of CD56+ cells were uncommon in early biopsies except for those with antibody-mediated rejection (AMR) only. On the other hand, high numbers of CD56+ cells were observed in late biopsies diagnosed as TCMR only, AMR only, and TCMR combined with AMR. In early biopsies, both CD56+ and CD163+ infiltrates correlated strongly with interstitial inflammation, tubulitis, and peritubular capillaritis (ptc) scores. The ci and ct scores, however, were correlated only with the number of CD56+ cells. In late biopsies, on the other hand, the number of CD56+ infiltrates was correlated only with ptc, while the number of CD163+ infiltrates was weakly correlated with any histologic lesion. Multivariable analyses showed that chronic active AMR and the number of CD56+ cells/10 HPF were independently associated with death-censored graft failure post-biopsy. The number of CD163+ cells was not correlated with any pathologic lesion and post-biopsy graft failure. CD56+ infiltrates were also associated with interstitial fibrosis and tubular atrophy.
  
  
  CONCLUSIONS
  Intragraft CD56+ cell infiltrates were significantly associated with AMR and subsequent poor clinical outcomes.
authors.affiliation: Department of Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
authors.forename: Sung
authors.initials: S
authors.lastname: Shin
authors.forename: Young Hoon
authors.initials: YH
authors.lastname: Kim
authors.forename: Yong Mee
authors.initials: YM
authors.lastname: Cho
authors.forename: Yangsoon
authors.initials: Y
authors.lastname: Park
authors.forename: Seungbong
authors.initials: S
authors.lastname: Han
authors.forename: Byung Hyun
authors.initials: BH
authors.lastname: Choi
authors.forename: Ji Yoon
authors.initials: JY
authors.lastname: Choi
authors.forename: Duck Jong
authors.initials: DJ
authors.lastname: Han
mesh_terms: D000328:Adult; D000906:Antibodies / Q000276:immunology; D015703:Antigens, CD / Q000276:immunology*; D015214:Antigens, Differentiation, Myelomonocytic / Q000276:immunology*; D001706:Biopsy; D019002:CD56 Antigen / Q000276:immunology*; D005260:Female; D006084:Graft Rejection / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000276:immunology* / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000601:surgery*; D016030:Kidney Transplantation; D007694:Killer Cells, Natural / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D055611:Natural Killer T-Cells / Q000276:immunology; D016016:Proportional Hazards Models; D011956:Receptors, Cell Surface / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D013997:Time Factors; D019737:Transplants / Q000276:immunology* / Q000473:pathology; D000098902:CD163 Antigen
chemical_list: D000906:Antibodies; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000098902:CD163 Antigen; D019002:CD56 Antigen; C522918:NCAM1 protein, human; D011956:Receptors, Cell Surface