Requirement of Interleukin‐17A for Systemic Anti–Candida albicansHost Defense in Mice

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ID: 302493
2004
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Abstract
T cells are required for normal host defense against fungal infection, and individuals with T cell.deficiency syndromes are highly susceptible to fungal pathogens. Interleukin (IL)-17A is a proinflammatory cytokine that interconnects myeloid and lymphoid host defense. The role of murine (m) IL-17A/mIL-17A receptor (R) interactions was evaluated in a murine model of systemic candidiasis. In response to systemic challenge with Candida albicans, expression of mIL-17A was induced, and IL-17AR knockout (IL-17AR−/−) mice had dosedependent, substantially reduced survival. Fungal burden in the kidneys of IL-17AR−/− mice was dramatically increased (25-fold at 96 h). In IL-17AR−/− mice, both mobilization of peripheral neutrophils and their influx to infected organs were significantly impaired and delayed. In vivo expression of mIL-17A protected normal mice from a lethal dose of C. albicans (100% at day 7 and 65% at day 42). The data suggest that the mIL- 17A/mIL-17AR system is required for normal fungal host defense in vivo. IL-17A could have potential as a therapeutic cytokine for systemic C. albicans infections in immunocompromised patients with cancer or advanced acquired immunodeficiency syndrome.
Reference Key
openalex_W2112133235 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Weitao Huang, Li Na, Paul L. Fidel, Paul Schwarzenberger
Journal The Journal of infectious diseases
Year 2004
DOI
10.1086/422329
URL
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