title: Characterisation of renal immune cell infiltrates in children with nephrotic syndrome.
abstract: There is increasing evidence that not only T cells but also B cells may play an important role in the pathogenesis of idiopathic nephrotic syndrome (NS). We have evaluated the infiltrating immune cells found in renal biopsies from 38 children with NS using immunohistochemistry techniques involving antibodies against T cells (CD3, CD4, CD8, FoxP3), B cells (CD20), macrophages (CD68) and follicular dendritic cells (CD21). Kidney biopsies with thin basement membrane disease were used as controls. We found higher numbers of interstitial CD3-positive T cells and macrophages in patients with focal segmental glomerulosclerosis (FSGS) than in those with minimal change glomerulopathy (MCGN) and in the controls, and significantly lower FoxP3-positive cells in patients with FSGS, MCGN and steroid-dependent NS than in the controls. Significantly higher numbers of glomerular B cells were found in FSGN patients than in MCGN patients and controls. Of note, in three patients who were later successfully treated with anti-CD20 antibody rituximab, the number of renal B cells was negligible in the preceding biopsy. In conclusion, the higher numbers of interstitial CD3-positive T cells in renal biopsies of pediatric patients with FSGS argue for a higher inflammatory activity. The significantly higher number of glomerular B cells in FSGS patients may indicate a particular pathogenetic role or epiphenomenon in this disease. However, patients with no interstitial or glomerular B cells could also benefit from rituximab treatment.
authors.affiliation: Klinik für Kinder und Jugendliche, Friedrich-Alexander-Universität Erlangen-Nürnberg, Loschgestrasse 15, 91054 Erlangen, Germany. kerstin.benz@uk-erlangen.de
authors.forename: Kerstin
authors.initials: K
authors.lastname: Benz
authors.forename: Maike
authors.initials: M
authors.lastname: Büttner
authors.forename: Katalin
authors.initials: K
authors.lastname: Dittrich
authors.forename: Valentina
authors.initials: V
authors.lastname: Campean
authors.forename: Jörg
authors.initials: J
authors.lastname: Dötsch
authors.forename: Kerstin
authors.initials: K
authors.lastname: Amann
mesh_terms: D000293:Adolescent; D015703:Antigens, CD / Q000378:metabolism; D001402:B-Lymphocytes / Q000378:metabolism / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D020566:Dendritic Cells, Follicular / Q000378:metabolism / Q000473:pathology; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D005923:Glomerulosclerosis, Focal Segmental / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007668:Kidney / Q000276:immunology / Q000473:pathology*; D007678:Kidney Glomerulus / Q000276:immunology / Q000473:pathology; D007962:Leukocytes / Q000378:metabolism / Q000473:pathology*; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D012157:Mononuclear Phagocyte System / Q000378:metabolism / Q000473:pathology*; D009402:Nephrosis, Lipoid / Q000276:immunology / Q000473:pathology*; D009404:Nephrotic Syndrome / Q000276:immunology / Q000473:pathology*; D012189:Retrospective Studies; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology
chemical_list: D015703:Antigens, CD; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors
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