Gene interactions and pathways from curated databases and text-mining

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CD86 — TLR4

Text-mined interactions from Literome

Mukhopadhyay et al., J Leukoc Biol 2004 : Conversely, studies with lipopolysaccharide (LPS)-deficient organisms and/or TLR-4 mutant mice showed that LPS and TLR-4 are at least partially required to induce CD80, CD86 , and MARCO, but LPS is not required to inhibit MHC-II
Weatherill et al., J Immunol 2005 : The dominant negative mutant of TLR4 or its downstream signaling components inhibits lauric acid induced expression of a CD86 promoter-reporter gene
van Duin et al., J Infect Dis 2007 (Influenza, Human) : We determined TLR induced monocyte CD80/CD86 expression by flow cytometry and vaccine antibody responses by hemagglutination inhibition
Funderburg et al., Proc Natl Acad Sci U S A 2007 : Here, we show that human beta-defensin-3 (hBD-3), an innate antimicrobial peptide, can induce expression of the costimulatory molecules CD80, CD86 , and CD40, on monocytes and myeloid dendritic cells in a TLR dependent manner
Martín-Vilchez et al., Br J Pharmacol 2008 (Hepatitis C) : AM3 promoted NF-kappaB activation in a TLR-4 dependent manner, and blocking TLR-4 activity attenuated the enhanced expression of CD80, CD83 and CD86 induced by AM3
Kim et al., Int Immunol 2009 : gamma-PGA induced the expression of IL-12p40, CD80 and CD86 in dendritic cells ( DC ) and macrophages in a Toll-like receptor-4 dependent manner, and the effect of gamma-PGA on T ( h ) 1/T ( h ) 2 development was dependent on the presence of antigen presenting cells (APC)
Siegemund et al., J Virol 2009 : In contrast, iPPVO induced TNF-alpha release and enhanced expression of MHC-I and CD86 but not of MHC-II by BMDC chiefly requires MyD88 but not TLR2 or TLR4
Jones et al., J Immunol 2010 : We compared the ability of progesterone to modulate murine bone marrow derived DC cytokine production ( IL-6 and IL-12 ) and costimulatory molecule expression ( CD40, CD80, and CD86 ) induced by either TLR3 or TLR4 ligation and determined whether activity was via the progesterone receptor (PR) or glucocorticoid receptor ( GR ) by comparative studies with the PR-specific agonist norgestrel and the GR agonist dexamethasone
Trujillo et al., J Investig Allergol Clin Immunol 2011 (Common Variable Immunodeficiency) : Interestingly, CD80 and CD86 expression on innate cells upon stimulation with TLR ligands was not altered in the patients although 3 of them exhibited low baseline levels of these surface molecules on monocytes compared to healthy controls