Abstract
Abstract Activated microglia can release a variety of proinflammatory cytokines that play a crucial role in the pathogenesis of multiple sclerosis (MS). IL-23 is a novel proinflammatory cytokine that shares the p40 subunit with IL-12 and is required for the induction of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. However, IL-23 expression and regulation in human microglia is poorly understood. Here we detected IL-23p19 mRNA expression on human microglia by northern blot and protein level by double-fluorescence immunostaining analysis. When the intracellular signaling pathway for p19 regulation was determined, we found that IL-23p19 expression in human microglia was significantly reduced by blocking the p38 MAP kinase pathway with either neutralizing antibodies or dominant-negative p38 transduction. Thus, human microglia inducibly express p19, and the p38 MAP kinase signaling pathway plays a major role in regulation of p19 expression.
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