Gene interactions and pathways from curated databases and text-mining

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IL12B — IL23R

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Morishima et al., Biochem Biophys Res Commun 2009 : TGF-beta is necessary for induction of IL-23R and Th17 differentiation by IL-6 and IL-23 ... Here, we found that IL-6 up-regulated IL-23R mRNA expression, and IL-6 and IL-23 synergistically augmented its protein expression ... However, unexpectedly, the up-regulation of IL-23R and induction of Th17 differentiation by IL-6 and IL-23 were almost completely inhibited by anti-TGF-beta ... These results suggest that the induction of IL-23R and Th17 differentiation by IL-6 and IL-23 is mediated through endogenously produced TGF-beta
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
Sieve et al., Eur J Immunol 2010 (Listeriosis) : Mechanistically, the IL-23 receptor was not required for this phenomenon, and IL-23 inhibited signaling through the IL-12 receptor by reducing IL-12 induced signal transducer and activator of transcription 4 ( STAT4 ) phosphorylation
Doisne et al., J Immunol 2011 : In this study, we show that the concomitant presence of IL-1 and IL-23 is crucial to induce a rapid and sustained IL-17A/F and IL-22 response by these cells that requires TCR-CD1d interaction and partly relies on IL-23 mediated upregulation of IL-23R and IL-1R1 expression
Sherlock et al., Nat Med 2012 (Arthritis, Experimental...) : We show here that IL-23 is essential in enthesitis and acts on previously unidentified IL-23 receptor (IL-23R) ( + ), RAR related orphan receptor ?t ( ROR-?t ) ( + ) CD3 ( + ) CD4 ( - ) CD8 ( - ), stem cell antigen 1 (Sca1) ( + ) entheseal resident T cells
Guo et al., PloS one 2012 : We provide evidence that IL23R-CHR can bind to IL-23 in a dose dependent manner in vitro, and block IL-23 signal by IL23R-CHR reducing the ROR?t expression, which in turn lowers the expression of IL-17/IL-22, thus protecting naive CD4+ T cells against Th17 development
Shen et al., PloS one 2013 : Variable expression of CD161, IL-23R and RORC affects IL-23 responsiveness and contributes to the inter-individual susceptibility to IL-23 mediated defenses and inflammatory processes