INTERLEUKIN-12 AND INTERFERON-GAMMA PRODUCTION IN CHILDHOOD IDIOPATHIC NEPHROTIC SYNDROME

Citation
V. Stefanovic et al., INTERLEUKIN-12 AND INTERFERON-GAMMA PRODUCTION IN CHILDHOOD IDIOPATHIC NEPHROTIC SYNDROME, Pediatric nephrology, 12(6), 1998, pp. 463-466
Citations number
21
Categorie Soggetti
Pediatrics,"Urology & Nephrology
Journal title
Pediatric nephrology
ISSN journal
0931041X → ACNP
Volume
12
Issue
6
Year of publication
1998
Pages
463 - 466
Database
ISI
SICI code
0931-041X(1998)12:6<463:IAIPIC>2.0.ZU;2-X
Abstract
Cellular immune disturbances, and T lymphocyte function in particular, have been previously implicated in idiopathic nephrotic syndrome (INS ) of childhood. There are different patterns of cytokine expression in various forms of glomerulonephritis, which suggests that local produc tion of these peptides plays an important role in the pathogenesis and progression of glomerulonephritis. To investigate T-cell and monocyte /macrophage cytokine production in INS, interleukin-12 (IL-12) and int erferon-gamma (IFN-gamma) production by peripheral blood mononuclear c ells (PBMC) of 11 children with steroid-sensitive nephrotic syndrome ( SSNS), 9 with focal segmental glomerulosclerosis (FSGS), and 17 health y controls was determined. Children with SSNS were studied in relapse, during corticosteroid treatment, and in stable remission, off cortico steroid treatment. IL-12 was not detected in serum, urine, and in supe rnatants of unstimulated PBMC. IL-12 production by concanavalin A (Con A)-stimulated PBMC of children with SSNS and FSGS was not different f rom controls. IFN-gamma production by Con A-stimulated PBMC was decrea sed in children with relapsing SSNS, both in relapse and and during co rticosteroid treatment. However, in stable remission it was similar to controls. Markedly decreased IFN-gamma production (P<0.001) was obser ved by pokeweed mitogen-stimulated PBMC of relapsing SSNS patients and moderately decreased production by PBMC of FSGS patients. This study has established a decreased production of IFN-gamma by PBMC of relapsi ng SSNS and FSGS patients, but does not allow differentiation between these two different conditions. IL-12 did not have a pathogenic role i n either SSNS or FSGS.