Immune response IL-23 signaling pathway
IL23 signaling pathway
Interleukin-23 ( IL-23 ) plays important role in expanding and maintaining theTh17 cell population, a novel T-cell subset involved in antimicrobial immune response andestablishment of many autoimmune diseases [1].
Interleukin-23 receptor ( IL-23 receptor ) is composed of Interleukin-12receptor beta-1 ( IL-12RB1 ) chain and Interleukin 23 alpha subunit p19 ( IL23A ).IL23A associates with Janus kinase 2 ( Jak2 ) and in a ligand-dependent manner withSignal transducer and activator of transcription STAT3 [2]. IL-12RB1interacts directly with Tyrosine kinase 2 ( Tyk2 ) [2].
IL-23 induced activation of STAT3 leads to direct binding of phosphorylated STAT3 toInterleukin-17 ( IL-17) and Interleukin 17F ( IL-17F ) promoters. [3]
IL-23 induced JAK2 activation triggers Phosphoinositide-3-kinase ( PI3K )/ RAC-alphaserine/threonine kinase ( AKT ) and Nuclear factor kappaB ( NF-kB ) pathways which arerequired for IL-17 production. PI3K/ AKT pathway is involved in STAT3 phosphorylationthrough an undetermined mechanism [4].
V-rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa lightpolypeptide gene enhancer in B-cells 3, p65 (avian) ( RelA (p65 NF-kB subunit) ) andNuclear factor of kappa light polypeptide gene enhancer in B-cells 1 (p105) ( NF-kB1(p50) ) bind IL17 promoter and up-regulate its expression [5].
Suppressor of cytokine signaling 3 ( SOCS3 ) may inhibit JAK2 activity, therebydecreasing IL-23 induced IL-17 and IL-17F expression [3].
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