V. Stefanovic et al., INTERLEUKIN-12 AND INTERFERON-GAMMA PRODUCTION IN CHILDHOOD IDIOPATHIC NEPHROTIC SYNDROME, Pediatric nephrology, 12(6), 1998, pp. 463-466
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.