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Defective phosphorylation of interleukin-18 receptor [beta] causes impaired natural killer cell function in systemic-onset juvenile idiopathic arthritis
Arthritis & Rheumatism, 09/01/09

de Jager W et al. – The mechanism of the impaired NK cell function in systemic-onset JIA involves a defect in IL-18R phosphorylation.

• The phenotype and function of NK cells from 10 healthy control subjects, 15 patients with polyarticular JIA, and 15 patients with systemic-onset JIA were characterized by staining and functional assays in vitro
• IL-18 ligand binding was visualized by fluorescence microscopy
• Phosphorylation of several MAP kinases and the IL-18 receptor (IL-18R) were visualized by Western blotting

• IL-18 from the plasma of systemic-onset JIA patients stimulated the activation of NK cells from healthy controls and bound its cognate receptor; however, NK cells from systemic-onset JIA patients failed to up-regulate cell-mediated killing molecules, such as perforin and interferon-, after IL-18 stimulation
• Tx with IL-18 did not induce the phosphorylation of receptor-activated MAP kinases in NK cells
• Alternate activation of NK cells by IL-12 induced NK cell cytotoxicity
• No additive effect of IL-18 in combination with IL-12 was noted in systemic-onset JIA patients
• Immunoprecipitation of IL-18R showed that NK cells from systemic-onset JIA could not phosphorylate this receptor after IL-18 stimulation

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