Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 4, Pages 2322-2328Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.4.2322
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The pathogenesis of sporadic cerebellar ataxia remains unknown. In this study, we demonstrate that proinflammatory cytokines, IL-18 and IL-1 beta, reciprocally regulate kainate-induced cerebellar ataxia in mice. We show that systemic administration of kainate activated IL-1 beta and IL-18 predominantly in the cerebellum of mice, which was accompanied with ataxia. Mice deficient in caspase-1, IL-1R type I, or MyD88 were resistant to kainate-induced ataxia, while IL-18- or IL-18R alpha-deficient mice displayed significant delay of recovery from ataxia. A direct intracerebellar injection of IL-1 beta-induced ataxia and intracerebellar coinjection of IL-18 counteracted the effect of IL-1 beta. Our data firstly show that IL-18 and IL-1 beta display differential direct regulation in kainate-induced ataxia in mice. Our results might contribute toward the development of a new therapeutic strategy for cerebellar ataxia in humans.
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