Genomic DNA of 54 Iranian patients with JIA and 139 healthy unrelated controls were typed for IL-2 (G/T at -330 and +166) as well as IFN-γ gene (A/T at +874), using polymerase chain reaction with sequence-specific primers method, and compared between patients and controls.
Compared with poly- and pauciarticular JIA, systemic JIA is associated with decreased NK cell function, more IFN-γ and less TNF-α secretion of NK cell and lower KIR2DS4 frequency.
Inflammatory macrophages are driven by interferon-γ (IFNγ), but studies have failed to demonstrate an IFN- induced gene signature in active systemic JIA.
Although PBMC from both patients with juvenile idiopathic arthritis and healthy controls produced interferon gamma in response to these peptides, only PBMC from patients with the disease produced interleukin 10.
Expression of transcripts encoding FucT-VII, interferon-gamma (IFN-gamma), and interleukin 12Rbeta2 (IL-12Rbeta2) were analyzed in T cells purified from synovial fluid (SF) and from peripheral blood (PB) of children with juvenile idiopathic arthritis (JIA) using kinetic reverse transcriptase polymerase chain reaction analysis.