T-cell subsets, interleukin-2 receptor expression and production of interleukin-2 in minimal change nephrotic syndrome.
This study was designed to investigate T-lymphocyte subsets interleukin-2 receptor (IL-2R) expression and IL-2 production in minimal change nephrotic syndrome (MCNS). Peripheral blood T-lymphocytes and IL-2R expression were analysed using fluorescein isothiocyanate-labelled CD3, CD4, CD8 and CD25 monoclonal antibodies with flow cytometry. IL-2 production was determined by enzyme immunoassay. Ten children with MCNS in relapse and in remission were evaluated. Thirteen healthy children served as controls. The patients in relapse demonstrated a moderate decrease in the total absolute lymphocyte counts and CD8(+) T-lymphocytes compared with controls (P < 0.05) and had a greatly increased IL-2R expression in freshly isolated, unstimulated peripheral lymphocytes compared with patients in remission and controls. While this was not statistically significant, IL-2R expression on cultured lymphocytes stimulated with phytohaemagglutinin was significantly elevated in relapse compared with those in remission and controls (P < 0.05). IL-2 production did not correlate well with IL-2R expression and there was no significant difference between the groups. Our results suggest that T-cell subset changes and high IL-2R expression on peripheral lymphocytes may indicate the presence of stimulated T-cell populations in MCNS which could contribute to the immunopathogenesis.
Topaloğlu
R
R
Department of Paediatric Nephrology, Hacettepe University, Faculty of Medicine, Ankara, Turkey.
Saatçi
U
U
Arikan
M
M
Canpinar
H
H
Bakkaloğlu
A
A
Kansu
E
E
D000293:Adolescent; D002478:Cells, Cultured; D002648:Child; D002675:Child, Preschool; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D009402:Nephrosis, Lipoid / Q000097:blood / Q000378:metabolism* / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000096:biosynthesis*; D016176:T-Lymphocyte Subsets / Q000378:metabolism / Q000473:pathology*
D015375:Receptors, Interleukin-2