Gene interactions and pathways from curated databases and text-mining

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CLEC7A — IL10

Text-mined interactions from Literome

Willment et al., J Immunol 2003 : Dectin-1 expression and function are enhanced on alternatively activated and GM-CSF treated macrophages and are negatively regulated by IL-10 , dexamethasone, and lipopolysaccharide
Dillon et al., J Clin Invest 2006 (Inflammation) : Induction of IL-10 is dependent on TLR2- and dectin-1 mediated activation of ERK MAPK via a mechanism independent of the activation protein 1 (AP-1) transcription factor c-Fos
Gow et al., J Infect Dis 2007 (Candidiasis...) : Dectin-1 induced cytokine production through the following 2 pathways : Syk dependent production of the T-helper ( Th ) 2-type anti-inflammatory cytokine interleukin-10 and Toll-like receptor-Myd88 dependent stimulation of monocyte derived proinflammatory cytokines, such as tumor necrosis factor-alpha
Mezger et al., J Infect Dis 2008 (Aspergillosis) : Silencing of dectin-1 resulted in reduced expression of proinflammatory cytokines ( tumor necrosis factor-alpha and interleukin-12 ), which was also reduced by anti-Dectin-1 antibody treatment prior to exposure to A. fumigatus, zymosan, or Candida albicans
Chaung et al., Vet Immunol Immunopathol 2009 : Zymosan enhanced dectin-1/TLR2/TLR4 expression and TNF-alpha/IL-10 production in all of three types of cell, whereas p-beta-glucan increased dectin-1/TLR4 and TNF-alpha/IL-12 production in AMs but inhibited IL-10 in mDCs
Bonfim et al., Med Mycol 2009 : There was a tendency towards an increased TLR2 and dectin-1 mRNA expression in response to fungal cells, mainly to Pb265. P. brasiliensis yeast cells induced the production of pro-inflammatory and anti-inflammatory cytokines, but the low ratio between TNF-alpha and IL-10 in response to zymosan and Pb265 indicates a balanced production of IL-10 and TNF-alpha, while Pb18 predominantly induced TNF-alpha secretion
Elcombe et al., PloS one 2013 : Furthermore, we show that MSKs regulate dectin-1 induced IL-10 production, and that this regulation is dependent on the ability of MSKs to phosphorylate the transcription factor CREB