title: T regulatory cell function in idiopathic minimal lesion nephrotic syndrome.
abstract: The purpose of this study was to test the hypothesis that, in idiopathic minimal lesion nephrotic syndrome (IMLNS), the T regulatory (T reg) cell suppressor mechanism is deficient, thereby enhancing cytokine release by T effector cells. Twenty-one patients with IMLNS, eight healthy controls and two patients with nephrotic syndrome and membranoproliferative glomerulonephritis were studied. The percentage of T reg cells was similar in the healthy controls and in patients with IMLNS in relapse or in remission. Thymidine incorporation in autologous T effector cells, as well as expression of the regulatory cytokine interleukin (IL)-10, was significantly reduced in patients in relapse when compared with patients in remission and healthy subjects. IL-2 expression was also reduced in patients in relapse but did not achieve statistical significance. In a different set of experiments, T cells, from subjects with IMLNS in remission, when stimulated with antiCD3-antiCD28 antibodies, secreted increased levels of cytokines. No such increase in cytokines was observed when cells from healthy controls were stimulated with same mitogen. The impaired T reg cell function observed in these patients may have pathogenic and therapeutic implications, because it could explain the persistence of the proposed pathogenic cytokines observed in the patients with IMLNS.
authors.affiliation: Department of Pediatrics, Division of Pediatric Nephrology, University of Florida,1600 SW Archer Road, Gainesville, FL 32610-0296, USA.
authors.forename: Carlos
authors.initials: C
authors.lastname: Araya
authors.forename: Leila
authors.initials: L
authors.lastname: Diaz
authors.forename: Clive
authors.initials: C
authors.lastname: Wasserfall
authors.forename: Mark
authors.initials: M
authors.lastname: Atkinson
authors.forename: Wei
authors.initials: W
authors.lastname: Mu
authors.forename: Richard
authors.initials: R
authors.lastname: Johnson
authors.forename: Eduardo
authors.initials: E
authors.lastname: Garin
mesh_terms: D000293:Adolescent; D000328:Adult; D018033:Antibodies, Bispecific / Q000276:immunology / Q000493:pharmacokinetics; D002452:Cell Count; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D005260:Female; D005434:Flow Cytometry; D015432:Glomerulonephritis, Membranoproliferative / Q000188:drug therapy / Q000276:immunology / Q000473:pathology; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D016753:Interleukin-10 / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009402:Nephrosis, Lipoid / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D012008:Recurrence; D012074:Remission Induction; D013491:Suppressor Factors, Immunologic / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D055815:Young Adult
chemical_list: D018033:Antibodies, Bispecific; D005938:Glucocorticoids; D007166:Immunosuppressive Agents; D013491:Suppressor Factors, Immunologic; D016753:Interleukin-10