Gene interactions and pathways from curated databases and text-mining

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CD80 — TLR4

Text-mined interactions from Literome

Farina et al., Int Immunol 2004 : Both TLR-ligands and inflammatory cytokines induced the expression of CD25, CD69, CD80 and, surprisingly, also of CD83, commonly regarded as an activation marker for mature dendritic cells ( DC )
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
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 ... The mean increase in TLR induced CD80 ( + ) monocytes was reduced in older, compared with young, adults by 68 % ( P=.0002 ), and each decile increase of CD80 ( + ) cells was associated with an 8.5 % increase in mean number of vaccine strains with a > or =4-fold titer increase ( P=.01 ) and a 3.8 % increase in mean number of strains with a postvaccine titer > or =1 : 64 ( P=.037 )
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)
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
Shimada et al., Nephrol Dial Transplant 2012 : We therefore evaluated the ability of TLR to induce CD80 in human cultured podocytes