TY  - JOUR
  - Canavan, M,McCarthy, C,Ben Larbi, N,Dowling, JK,Collins, L,O'Sullivan, F,Hurley, G,Murphy, C,Quinlan, A,Moloney, G,Darby, T,MacSharry, J,Kagechika, H,Moynagh, P,Melgar, S,Loscher, CE
  - 2014
  - October
  - Innate Immunity
  - Activation of liver X receptor suppresses the production of the IL-12 family of cytokines by blocking nuclear translocation of NF-kappa Bp50
  - Validated
  - Altmetric: 1 ()
  - Liver X receptor dendritic cells interleukin-12 NF-kappa B NF-KAPPA-B INFLAMMATORY-BOWEL-DISEASE DENDRITIC CELLS PPAR-GAMMA C-REL INDUCTION TRANSCRIPTION MACROPHAGES EXPRESSION HOMEOSTASIS
  - 20
  - 675
  - 687
  - There is now convincing evidence that liver X receptor (LXR) is an important modulator of the inflammatory response; however, its mechanism of action remains unclear. This study aimed to examine the effect of LXR on the IL-12 family of cytokines and examined the mechanism by which LXR exerted this effect. We first demonstrated that activation of murine-derived dendritic cells (DC) with a specific agonist to LXR enhanced expression of LXR following activation with LPS, suggesting a role in inflammation. Furthermore, we showed LXR expression to be increased in vivo in dextrane sulphate sodium-induced colitis. LXR activation also suppressed production of IL-12p40, IL-12p70, IL-27 and IL-23 in murine-derived DC following stimulation with LPS, and specifically targeted the p35, p40 and EBI3 subunits of the IL-12 cytokine family, which are under the control of the NF-kappa B subunit p50 (NF-kappa Bp50). Finally, we demonstrated that LXR can associate with NF-kappa Bp50 in DC and that LXR activation prevents translocation of the p50 subunit into the nucleus. In summary, our study indicates that LXR can specifically suppress the IL-12 family of cytokines though its association with NF-kappa Bp50 and highlights its potential as a therapeutic target for chronic inflammatory diseases.
  - 10.1177/1753425913501915
DA  - 2014/10
ER  - 

@article{V279268961,
   = {Canavan,  M and McCarthy,  C and Ben Larbi,  N and Dowling,  JK and Collins,  L and O'Sullivan,  F and Hurley,  G and Murphy,  C and Quinlan,  A and Moloney,  G and Darby,  T and MacSharry,  J and Kagechika,  H and Moynagh,  P and Melgar,  S and Loscher,  CE },
   = {2014},
   = {October},
   = {Innate Immunity},
   = {Activation of liver X receptor suppresses the production of the IL-12 family of cytokines by blocking nuclear translocation of NF-kappa Bp50},
   = {Validated},
   = {Altmetric: 1 ()},
   = {Liver X receptor dendritic cells interleukin-12 NF-kappa B NF-KAPPA-B INFLAMMATORY-BOWEL-DISEASE DENDRITIC CELLS PPAR-GAMMA C-REL INDUCTION TRANSCRIPTION MACROPHAGES EXPRESSION HOMEOSTASIS},
   = {20},
  pages = {675--687},
   = {{There is now convincing evidence that liver X receptor (LXR) is an important modulator of the inflammatory response; however, its mechanism of action remains unclear. This study aimed to examine the effect of LXR on the IL-12 family of cytokines and examined the mechanism by which LXR exerted this effect. We first demonstrated that activation of murine-derived dendritic cells (DC) with a specific agonist to LXR enhanced expression of LXR following activation with LPS, suggesting a role in inflammation. Furthermore, we showed LXR expression to be increased in vivo in dextrane sulphate sodium-induced colitis. LXR activation also suppressed production of IL-12p40, IL-12p70, IL-27 and IL-23 in murine-derived DC following stimulation with LPS, and specifically targeted the p35, p40 and EBI3 subunits of the IL-12 cytokine family, which are under the control of the NF-kappa B subunit p50 (NF-kappa Bp50). Finally, we demonstrated that LXR can associate with NF-kappa Bp50 in DC and that LXR activation prevents translocation of the p50 subunit into the nucleus. In summary, our study indicates that LXR can specifically suppress the IL-12 family of cytokines though its association with NF-kappa Bp50 and highlights its potential as a therapeutic target for chronic inflammatory diseases.}},
   = {10.1177/1753425913501915},
  source = {IRIS}
}