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- W1585461212 abstract "Abstract IL-23, a heterodimeric cytokine composed of the p40 subunit of IL-12 and a novel p19 subunit, has been shown to be a key player in models of autoimmune chronic inflammation. To investigate the role of IL-23 in host resistance during chronic fungal infection, wild-type, IL-12- (IL-12p35−/−), IL-23- (IL-23p19−/−), and IL-12/IL-23- (p40-deficient) deficient mice on a C57BL/6 background were infected with Cryptococcus neoformans. Following infection, p40-deficient mice demonstrated higher mortality than IL-12p35−/− mice. Reconstitution of p40-deficient mice with rIL-23 prolonged their survival to levels similar to IL-12p35−/− mice. IL-23p19−/− mice showed a moderately reduced survival time and delayed fungal clearance in the liver. Although IFN-γ production was similar in wild-type and IL-23p19−/− mice, production of IL-17 was strongly impaired in the latter. IL-23p19−/− mice produced fewer hepatic granulomata relative to organ burden and showed defective recruitment of mononuclear cells to the brain. Moreover, activation of microglia cells and expression of IL-1β, IL-6, and MCP-1 in the brain was impaired. These results show that IL-23 complements the more dominant role of IL-12 in protection against a chronic fungal infection by an enhanced inflammatory cell response and distinct cytokine regulation." @default.
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- W1585461212 date "2006-01-15" @default.
- W1585461212 modified "2023-10-06" @default.
- W1585461212 title "IL-23 Enhances the Inflammatory Cell Response in <i>Cryptococcus neoformans</i> Infection and Induces a Cytokine Pattern Distinct from IL-12" @default.
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- W1585461212 doi "https://doi.org/10.4049/jimmunol.176.2.1098" @default.
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