title: Small bowel T cells, HLA class II antigen DR, and GroEL stress protein in IgA nephropathy.
abstract: BACKGROUND
  Previous studies suggest that intestinal mucosa may be involved in the pathogenesis of IgA nephropathy (IgAN). To further clarify this involvement, we investigated whether or not IgAN patients have small bowel mucosal findings suggestive of inflammation and stress.
  
  
  METHODS
  Seventeen patients with IgAN underwent gastroscopic examination. Fresh small bowel biopsy specimens were frozen, and in cryosections, the proportion of alphabeta and gammadelta receptors bearing T cells and CD3+ T cells were quantitated immunohistochemically. The expression of HLA class II antigen DR (HLA-DR) and human GroEL stress-protein homologue was similarly quantitated. In an avidin-biotin peroxidase technique, the following monoclonal primary antibodies were used: anti-beta-chain (betaF1), anti-delta-chain (TCRdelta1), anti-CD3 (Leu4), anti-constant fragment of HLA-DR (L243), and anti-GroEL (ML30). Twenty-nine patients who had undergone gastroscopy because of dyspepsia served as controls.
  
  
  RESULTS
  In all specimens, the mucosal architecture was normal. The amount of gammadelta T cells and the total amount of T cells, as indicated by CD3+ positivity, were both significantly increased in IgAN. The number of alphabeta T cells was also higher in the IgAN patients. Villous epithelium of the IgAN patients disclosed a significant increase in the expression of HLA-DR antigen and GroEL stress protein.
  
  
  CONCLUSIONS
  Our results suggest that ongoing small bowel inflammation and stress are present in IgAN. Despite normal morphology, there is reason to believe that the small bowel mucosa is involved in the pathogenesis of IgAN.
authors.affiliation: Pathology Unit, Department of Internal Medicine, Tampere University Hospital, Finland. immo.rantala@tays.fi
authors.forename: I
authors.initials: I
authors.lastname: Rantala
authors.forename: P
authors.initials: P
authors.lastname: Collin
authors.forename: K
authors.initials: K
authors.lastname: Holm
authors.forename: H
authors.initials: H
authors.lastname: Kainulainen
authors.forename: J
authors.initials: J
authors.lastname: Mustonen
authors.forename: M
authors.initials: M
authors.lastname: Mäki
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D018834:Chaperonin 60 / Q000378:metabolism*; D005260:Female; D005922:Glomerulonephritis, IGA / Q000276:immunology* / Q000473:pathology*; D006684:HLA-DR Antigens / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D007413:Intestinal Mucosa / Q000276:immunology / Q000473:pathology; D007421:Intestine, Small / Q000276:immunology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000473:pathology*
chemical_list: D018834:Chaperonin 60; D006684:HLA-DR Antigens; D016692:Receptors, Antigen, T-Cell, gamma-delta