title: Intrarenal IFN-γ mRNA expression differentiates clinical and subclinical glomerulitis in renal transplant recipients.
abstract: BACKGROUND
  Transplant glomerulitis, characterized by mononuclear cell infiltration of glomeruli, is likely to occur during clinical or subclinical antibody-mediated rejection.
  
  
  METHODS
  To determine whether T-cell phenotype influences the clinical presentation of this pathologic condition, we used reverse transcription quantitative polymerase chain reaction to analyze expression of Treg cells (Foxp3), cytotoxic CD8 T cells (Granzyme B), Th1 cells (INF-γ,T Bet), Th2 cells (GATA3, IL-4), and Th17 pathway (IL-17). Our study included 20 renal transplant recipients exhibiting subclinical glomerulitis (SG) diagnosed after a routine 3-month posttransplant biopsy. Results were compared with those observed in 22 patients with normal routine biopsies at 3 months (N) and 17 patients with clinical glomerulitis occurring during early acute renal dysfunction within the first year after transplantation in a context of acute antibody-mediated rejection.
  
  
  RESULTS
  Our results show that expression of IL-4 mRNA was significantly higher in SG patients than in N patients (P = 0.02). Expression of IFN-γ was significantly higher in patients with clinical glomerulitis than in patients with SG (P<0.001) and was associated with a clinical expression of glomerulitis.
  
  
  CONCLUSIONS
  Our results suggest that the balance of Th1/Th2 is likely to differentiate clinical expression of transplant glomerulopathy. They also indicate that therapeutic approaches in cases of SG should be defined with caution and take into account transcriptional criteria.
authors.affiliation: Univ Lille Nord de France F-59000, France.
authors.forename: David
authors.initials: D
authors.lastname: Buob
authors.forename: Marc
authors.initials: M
authors.lastname: Hazan
authors.forename: Sebastien
authors.initials: S
authors.lastname: Homs
authors.forename: Marie
authors.initials: M
authors.lastname: Matignon
authors.forename: Hicham
authors.initials: H
authors.lastname: Mansour
authors.forename: Vincent
authors.initials: V
authors.lastname: Audard
authors.forename: Dominique
authors.initials: D
authors.lastname: Desvaux
authors.forename: Philippe
authors.initials: P
authors.lastname: Remy
authors.forename: Christian
authors.initials: C
authors.lastname: Noel
authors.forename: Sylvie
authors.initials: S
authors.lastname: Bastuji-Garin
authors.forename: José
authors.initials: J
authors.lastname: Cohen
authors.forename: Philippe
authors.initials: P
authors.lastname: Lang
authors.forename: Philippe
authors.initials: P
authors.lastname: Grimbert
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D003937:Diagnosis, Differential; D005260:Female; D005921:Glomerulonephritis / Q000175:diagnosis* / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism*; D015847:Interleukin-4 / Q000378:metabolism; D007668:Kidney / Q000378:metabolism* / Q000473:pathology; D016030:Kidney Transplantation; D007963:Leukocytes, Mononuclear / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism*; D012189:Retrospective Studies; D018417:Th1 Cells / Q000378:metabolism / Q000473:pathology; D018418:Th2 Cells / Q000378:metabolism / Q000473:pathology; D014180:Transplantation
chemical_list: D015415:Biomarkers; D012333:RNA, Messenger; D015847:Interleukin-4; D007371:Interferon-gamma