Abstract

Cytokines are small-molecular weight proteins involved in regulating inflammation, proliferation and differentiation of immunocompetent cells, as well as effector functions. IL-1β and TNFα are among the most powerful inducers of the inflammatory response. Production of proinflammatory cytokines comprises normal response to infection and represents an arm of various autoimmune disease pathogenesis. It is worth comparing cytokine production in autoimmune and infectious diseases to determine features of cytokine profile. The aim of the study was to evaluate proinflammatory cytokines IL-1β and TNFα produced by blood cells in children with autoimmune and infectious diseases. 194 children, aged 2-17 years, were examined: 99 patients with juvenile idiopathic arthritis; 26 patients with unspecified reactive arthropathy; 14 children with systemic lupus erythematosus; 24 children with chronic viral hepatitis C; 33 healthy children. Heparinized blood samples were diluted with a glutamine-containing culture medium RPMI-1640, samples with/without phytohemagglutinin stimulation were prepared as well. Samples of diluted blood were incubated for 24 hours (37 °C, 5% CO2). The concentrations of IL-1β and TNFα in the cell culture supernatants were determined by ELISA. It was found that groups of patients with rheumatic diseases (systemic lupus erythematosus, juvenile idiopathic arthritis and unspecified reactive arthropathy) were featured with spontaneous production of IL-1β and TNFα at higher level than in control, and the stimulated synthesis of IL-1β was lower. In patients with chronic viral hepatitis C, the spontaneous concentration IL-1β and TNFα and the stimulated concentration of IL-1β did not differ those ones found in healthy children. Stimulated TNFα production in patients with juvenile idiopathic arthritis, unspecified reactive arthropathy, and hepatitis C was significantly higher than in control group. More intensive spontaneous production IL-1β and TNFα in groups of patients with rheumatic diseases indicates previous activation of immunocompetent cells. Decreased stimulated IL-1β production in groups with various diseases points at exhaustion of immunocompetent cell functional reserve due to chronic activation.

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