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IL23A — STAT3

Pathways - manually collected, often from reviews:

• NCI Pathway Database IL23-mediated signaling events: STAT3 (STAT3) → IL23/IL23R/JAK2/TYK2 complex (IL23A-IL12B-IL23R-IL12RB1-JAK2-TYK2) (modification, collaborate)
  Parham et al., J Immunol 2002, Cho et al., J Immunol 2006
  Evidence: mutant phenotype, physical interaction, other species
• NCI Pathway Database IL23-mediated signaling events: STAT3 (STAT3) → IL23/IL23R/JAK2/TYK2 complex (IL23A-IL12B-IL23R-IL12RB1-JAK2-TYK2) (modification, collaborate)
  Oppmann et al., Immunity 2000, Parham et al., J Immunol 2002
  Evidence: assay, physical interaction

Text-mined interactions from Literome

Chen et al., Proc Natl Acad Sci U S A 2006 : By contrast, Socs3 was found to be a major regulator of IL-23 mediated Stat3 phosphorylation and Th17 generation, and Stat3 directly binds to the IL-17A and IL-17F promoters
Li et al., J Immunol 2006 (Encephalomyelitis, Autoimmune, Experimental) : Indeed, in the present study we found that bone marrow derived DCs transduced with SOCS-3 significantly inhibited IL-12 induced activation of Stat4 and IL-23 induced activation of Stat3
Caruso et al., Eur J Immunol 2008 (Helicobacter Infections) : Treatment of normal gastric lamina propria mononuclear cells ( LPMC ) with IL-23 enhanced Stat3 activation and IL-17 secretion, and pharmacological inhibition of Stat3 prevented IL-23-driven IL-17 synthesis
Stewart et al., Cancer Cell 2009 (Neoplasms) : In this issue of Cancer Cell, Kortylewski et al. show that in the tumor microenvironment, STAT3 enhances the expression of the protumor cytokine IL-23 in macrophages but inhibits the antitumor cytokine IL-12 in dendritic cells
Kortylewski et al., Cancer Cell 2009 (Neoplasms) : Stat3 induces expression of IL-23 , which is mainly produced by tumor associated macrophages, via direct transcriptional activation of the IL-23/p19 gene
Staschke et al., J Immunol 2009 (Encephalomyelitis, Autoimmune, Experimental) : Furthermore, the absence of IRAK4 kinase activity blocked induction of IL-23R expression, STAT3 activation by IL-23 , and Th17 cytokine expression in differentiated Th17 cells
Paradowska-Gorycka et al., Scand J Immunol 2010 (Arthritis, Rheumatoid...) : IL-23 binding to an IL-23 receptor expressed on dendritic cells, macrophages and monocytes triggers the activation of Jak2 and Tyk2, which in turn phosphorylates STAT1, STAT3, STAT4 and STAT5 as well as induce formation of STAT3-STAT4 heterodimers
Jager et al., J Neuroimmunol 2011 (Encephalomyelitis, Autoimmune, Experimental) : SOCS1-KIR also blocked IL-23 and IL-17A activation of STAT3
Di Meglio et al., PloS one 2011 (Immune System Diseases) : However, IL-23 mediated Th17 cell effector function was impaired, as Th17 cells from A allele carriers had significantly reduced IL-23 induced IL-17A production and STAT3 phosphorylation compared to G allele carriers
Balamayooran et al., Infect Immun 2011 (Escherichia coli Infections...) : RIP2 ( -/- ) mice also show reduced IL-6 and IL-23 levels in the lungs, along with decreased activation of STAT3 after infection
Pidasheva et al., PloS one 2011 (Genetic Predisposition to Disease...) : IL23R ( Q381 ) was associated with reduced STAT3 phosphorylation upon stimulation with IL-23 and decreased number of IL-23 responsive T-cells
Floss et al., J Biol Chem 2013 : In contrast to IL-6 induced short term STAT3 phosphorylation, cellular activation by IL-23 resulted in a slower but long term STAT3 phosphorylation, indicating that the IL-23R might not be a major target of negative feedback inhibition by suppressor of cytokine signaling (SOCS) proteins