PI3K-mediated negative feedback regulation of IL-12 production in DCs

By T. Fukao, M. Tanabe, Y. Terauchi, T. Ota, S. Matsuda, T. Asano, Takashi Kadowaki, T. Takeuchi, S. Koyasu. Nature Immunology, 2002

619 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/98b0789b451236c246d17331650e42c5ccb8864d

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In Immunology

1. Shizuo Akira
2. Luke A. O'Neill
3. K. Takeda
4. Aly Karsan
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Citations in the corpus

• Toll-like receptor–mediated cytokine production is differentially regulated by glycogen synthase kinase 3 (2005, background): “to limit production of tumor necrosis factor (TNF) and interleukin 12 (IL-12”
• Lipopolysaccharide signaling in endothelial cells (2006, background): “125 Activation of PI3K also reduces MyD88-dependent production of the proinflammatory molecules IL-12 in dendritic cells and TNF α in monocytes”
• Toll-like receptor signalling (2004, background): “However, recent studies using mice that lack the p85 regulatory subunit showed an increased production of IL-12 by DCs, possibly because of enhanced activation of the p38 MAPK, indicating that PI3K might have a negative role in TLR signalling in DC”
• Negative regulation of Toll-like receptor-mediated immune responses (2005, background): “IL-12 synthesis by dendritic cells from PI3K-deficient mice was markedly increased in response to the TLR4, TLR2 and TLR9 ligands LPS, peptidoglycan and CpG DNA, respectivel”
• The role of immune dysfunction in the pathophysiology of autism (2011, positive): “Expression profiling of postmortem brain tissue from ASD individuals revealed increased messenger RNA transcript levels of several immune system associated genes, further implicating neuroinflammatory processes in this disorder (Garbett et al., 2008).”
• Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “Thus, activation of the PI-3K-Akt pathway suppresses LPS-activated MAPK and NF-kB signaling cascades in monocytes and dendritic cells, resulting in decreased production of TNF-a and other cytokines (Fukao et al., 2002; Guha and Mackman, 2002).”