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See Latest ArticlesDefective 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.
Methods- 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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