The Evolving View of IL-17-Mediated Immunity in Defense Against Mucocutaneous Candidiasis in Humans.
作者： Beáta Soltész , Beáta Tóth , Adrien Katalin Sarkadi , Melinda Erdős , László Maródi
DOI: 10.3109/08830185.2015.1049345
关键词: Innate immune system 、 Mucocutaneous Candidiasis 、 Immunity 、 STAT protein 、 STAT3 、 Pattern recognition receptor 、 STAT1 、 Autoimmune polyendocrine syndrome 、 Biology 、 Immunology
摘要: The discovery of interleukin (IL)-17-mediated immunity has provided a robust framework upon which our current understanding the mechanism involved in host defense against mucocutaneous candidiasis (CMC) been built. Studies have shed light on how pattern recognition receptors expressed by innate immune cells recognize various components Candida cell wall. Inborn errors affecting IL-17+ T differentiation recently defined, such as deficiencies signal transducer and activator transcription (STAT)3, STAT1, IL-12Rβ1 IL-12p40, caspase recruitment domain 9. Impaired receptor-ligand coupling was identified patients with IL-17F IL-17 receptor A (IL17RA) deficiency autoimmune polyendocrine syndrome (APS) type 1. Mutation nuclear factor kappa B (ACT) 1 described cause impaired IL-17R-mediated signaling. CMC may be part complex clinical phenotype like STAT3, IL-12Rβ1/IL-12p40 APS-1 or ma...
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