title: HLA-DR display by renal tubular epithelium and phenotype of infiltrate in interstitial nephritis.
abstract: Renal tubular display of HLA-DR was estimated semi-quantitatively in 28 biopsies from 27 patients with various forms of tubulointerstitial nephritis (10 following use of non-steroidal anti-inflammatory drugs) using a monoclonal anti-MHC class II non-polymorphic antibody (DK-22). Normal donor kidneys and biopsies from patients with minimal-change nephrotic syndrome were examined as controls. The phenotype of infiltrating cells was also studied quantitatively, using monoclonal antibodies on frozen biopsy tissue; the number of cells infiltrating the interstitium was counted per tubular cross-section. Display of HLA-DR was seen in up to 5% of control tubular cells, but up to 100% expressed HLA-DR in tubulointerstitial nephritis biopsies. There was a correlation between the expression of HLA-DR and the severity of both tubular atrophy and tubulointerstitial fibrosis judged semi-quantitatively by optical microscopy. In controls up to 50 leucocytes per tubular cross-section were evident, but in patients with tubulointerstitial nephritis up to 1500 were observed, approximately 50% being T-lymphocytes, the majority expressing the helper phenotype except in early, active drug-induced tubulointerstitial nephritis; the remainder were mostly monocytes. There were no qualitative differences between the different causes of tubulointerstitial nephritis. Tubular DR expression correlated with the number of DR-positive cells in the interstitium, but not with total leucocytes or T-lymphocytes. HLA-DR tubular expression was greater in the early stages than late stages of NSAID-induced tubulointerstitial nephritis, but this relationship was not present in the group as whole. HLA-DR expression by renal tubular epithelial cells may play a role in localising or amplifying tubular injury in tubulointerstitial nephritis.
authors.affiliation: Department of Pathology, United Medical School, London, UK.
authors.forename: H F
authors.initials: HF
authors.lastname: Cheng
authors.forename: F
authors.initials: F
authors.lastname: Nolasco
authors.forename: J S
authors.initials: JS
authors.lastname: Cameron
authors.forename: G
authors.initials: G
authors.lastname: Hildreth
authors.forename: G H
authors.initials: GH
authors.lastname: Neild
authors.forename: B
authors.initials: B
authors.lastname: Hartley
authors.forename: G
authors.initials: G
authors.lastname: Neild
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D000911:Antibodies, Monoclonal; D002648:Child; D004848:Epithelium / Q000276:immunology; D005110:Extracellular Space / Q000276:immunology; D005260:Female; D006684:HLA-DR Antigens / Q000032:analysis*; D006801:Humans; D007678:Kidney Glomerulus / Q000276:immunology; D007684:Kidney Tubules / Q000276:immunology*; D007963:Leukocytes, Mononuclear / Q000032:analysis; D008297:Male; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000276:immunology*; D010641:Phenotype; D013601:T-Lymphocytes / Q000032:analysis
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D006684:HLA-DR Antigens