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CD86 — IRF6

Text-mined interactions from Literome

Foss et al., Infect Immun 1999 : We found that CT and LPS differentially regulated the expression of interleukin-12 (IL-12) and CD80-CD86 but not that of IL-1beta ... LPS and CT each induced IL-1beta expression in macrophages, while only LPS induced IL-12 and only CT induced CD80-CD86 ... These differences were markedly potentiated in gamma interferon ( IFN-gamma ) -treated macrophages, in which LPS potently induced IL-12 and CD80-CD86 expression
Li et al., Scand J Immunol 2000 : Lipopolysaccharide (LPS) treatment induced the upregulation of CD40, CD80, CD86 and the T-cell stimulatory capacity in IL-4-DCs and, to a lesser extent, in the IL-7-DCs whereas GM-CSF-DCs responded very poorly to such treatment
Heinzelmann et al., Immunopharmacology 2000 : On monocytes, LPS and MDP increased surface expression of human leukocyte antigen-DR ( HLA-DR ), CD18, CD54 ( intercellular adhesion molecule-1, ICAM-1 ), and CD86 ( B7-2 )
Arrighi et al., J Immunol 2001 (Dermatitis, Allergic Contact) : SB203580, an inhibitor of the p38 MAPK, but not the extracellular signal regulated kinase l/2 pathway blocker PD98059, inhibited the up-regulation of CD1a, CD40, CD80, CD86 , HLA-DR, and the DC maturation marker CD83 induced by LPS and TNF-alpha
Seixas et al., Eur J Immunol 2001 : In contrast to some strains of the human parasite, P. falciparum, P.c. chabaudi ( AS ) did not inhibit the up-regulation of MHC class II, CD86 or CD40 induced by LPS
Brodskyn et al., Infect Immun 2002 : LPS induced HLA-DR, CD83, and CD86 up-regulation was significantly inhibited by GIPL
Weigt et al., Immunobiology 2003 : MALP-2 and LPS stimulation induced the expression of CD83 and increased the expressions of CD80, CD86 , HLA-ABC and CD40
Mahanonda et al., J Dent Res 2004 (Periodontitis) : LPS stimulation resulted in a dose dependent up-regulation of CD40, CD80, and CD86 on monocytes, and up-regulation of CD69 on NK cells and gamma delta T-cells in both the periodontitis and non-periodontitis groups
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
Chen et al., J Immunol 2004 : PS liposomes inhibited the up-regulation of HLA-ABC, HLA-DR, CD80, CD86 , CD40, and CD83, as well as the production of IL-12p70 by human DCs in response to LPS
Nakahara et al., Int Immunol 2004 : SP600125, a specific inhibitor of JNK, inhibited the LPS induced up-regulation of CD80, CD83, CD86 and CD54, but augmented the up-regulation of HLA-DR. SP600125 slightly inhibited the down-regulation of FITC-dextran uptake during DC maturation
Dimayuga et al., J Neuroimmunol 2005 (Encephalitis) : Specifically, the effects of 17beta-estradiol on basal and LPS induced surface staining of Class I and II MHC, as well as CD40, CD80, CD86 , CD152, CD28, CD8, CD11b, Fas, FasL, and also ERalpha and ERbeta, were examined in N9 microglial cells
Zhou et al., Eur J Immunol 2005 : For example, LPS induced up-regulation of CD80 ( B7.1 ) and CD86 ( B7.2 ) is abrogated in antigen presenting cells (APC) deficient in TRIF or TRAM, two adaptors that are responsible for TLR4 mediated production of Type I IFN
Kang et al., J Immunol 2005 : The costimulation of DCs with WKYMVm and LPS dramatically inhibited LPS induced IL-12 production, CD86 and HLA-DR surface expression, and DC-mediated T cell proliferation
Vassallo et al., J Immunol 2005 : Conditioning of DCs with CSE also suppressed LPS mediated induction of CD40, CD80, and CD86 , and suppressed maturation associated CCR7 expression
Strengell et al., J Leukoc Biol 2006 : Pretreatment of immature DCs with IL-21 inhibited LPS stimulated DC maturation and expression of CD86 and human leukocyte antigen class II ( HLAII )
Wikstrom et al., J Immunol 2006 : Both LPS and CT stimulated increases in CD80 and CD86 expression on OVA+CD8alpha ( low ) DC
Zhou et al., J Immunol 2007 : Iloprost and cicaprost also suppressed LPS induced expression of CD86 , CD40, and MHC class II molecules by BMDCs and inhibited the ability of BMDCs to stimulate Ag-specific CD4 T cell proliferation and production of IL-5 and IL-13
Chen et al., Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi 2007 : LPS stimulation increased the expression of CD80, CD86 and MHC-II in the cytomembrane of DCs, the concentration of TNF-alpha, IFN-gamma and IL-12 in the supernatant in control group
Messmer et al., Mol Med 2006 (Opioid-Related Disorders) : Chronic morphine treatment ( 10 ( -8 ) to 10 ( -12 ) M ) during the development of DCs from monocytes augmented LPS induced upregulation of HLA-DR, CD86 , CD80, and CD83 and increased the T cell stimulatory capacity of DCs, which could be inhibited by naloxone, an opioid receptor antagonist
Zhang et al., Chin Med J (Engl) 2007 : LPS induced up-regulation of CD86 was moderately suppressed by LXA ( 4 ) but no obvious change of CD80 was observed
Sá-Nunes et al., J Immunol 2007 : Moreover, we have found that I. scapularis saliva ( dilution 1/200 ; approximately 10 nM PGE ( 2 ) ) marginally inhibited LPS induced CD40, but not CD80, CD86 , or MHC class II expression
Jiang et al., J Immunol 2007 : NGF could markedly promote LPS induced expression of HLA-DR, CD40, CD80, CD83, CD86 , CCR7, secretion of IL-12p40 and proinflammatory cytokines IL-1, IL-6, TNF-alpha, and the T cell stimulating capacity of MoDCs, indicating that NGF can promote LPS induced DC maturation
Wang et al., J Immunol 2007 : LPS stimulation of splenic DCs in vivo resulted in prolonged CD80/CD86 expression on WSX-1-deficient DCs over wild-type DCs
Zaru et al., J Biol Chem 2008 : However, LPS induced expression of class II major histocompatibility complex and CD86 were elevated in PDK1 ( fl/- ) BMDC and PDK1 ( fl/- ) spleen DC produced more interleukin-10 and -12, implying an attenuating role for PDK1
Santander et al., Biomedica 2007 (Chagas Disease) : KMP-1 1 protein does not affect the maturation of dendritic cells, but in the presence of LPS the K1 peptide leads to a decreased expression of CD86 and CD83 as well as interleukin-12 production, This phenomenon may be associated with an impaired T cell stimulation
Xu et al., Immunology 2008 : Following LPS stimulation, up-regulation of the surface markers CD40, CD86 , I-Ad, immunoglobulin M, CD54 and interleukin-10 production, accompanied by down-regulation of CD5 and CD184 ( CXCR4 ) were observed in a LPS dose dependent manner
Lu et al., Int Immunopharmacol 2008 : In the presence of LPS , VIP also dose dependently up-regulated the expression of CD80, CD86 , CD54 and CD40, and down-regulated the expression of Ia ( b )
Ohman et al., Neurogastroenterol Motil 2009 (Irritable Bowel Syndrome) : B cells of IBS patients displayed an impaired ability to increase expression of CD80, but not CD86 , in response to both LPS as well as probiotic bacteria stimulations
Agrawal et al., Nephrol Dial Transplant 2010 (Kidney Failure, Chronic) : The magnitude of the LPS induced up-regulation of CD86 was comparable among the study groups as well as pre- and post-dialysis samples
North et al., Toxicological sciences : an official journal of the Society of Toxicology 2010 : TCDD significantly impaired LPS activated expression of major histocompatibility complex class II, cluster of differentiation (CD)69, CD80, and CD86
Hammarfjord et al., J Leukoc Biol 2010 : LPS induced up-regulation of CD86 was normal ; however, CD40 up-regulation was suppressed after TLR-4 stimulation at 28°C
Marim et al., PloS one 2010 : We compared BMDM obtained from fresh and frozen BM cells and found that both are similarly able to trigger the expression of CD80 and CD86 in response to LPS or infection with the intracellular bacteria Legionella pneumophila
Lin et al., Stem Cell Rev 2011 : Both ES and iPS derived DCs expressed activation molecules ( CD86 , CD80 ) in response to LPS stimulation and stimulated T cell proliferation in a mixed lymphocyte reaction (MLR)
Tavano et al., J Innate Immun 2011 : Suboptimal stimulatory doses ( 5-10 µM ) of apidaecin partially inhibited the lipopolysaccharide (LPS) induced increase in major histocompatibility complex class II ( MHCII ) and CD86 in macrophages, and the release of selected cytokines/chemokines by both macrophages [ interleukin (IL)-6 and tumor necrosis factor (TNF)-a ] and monocytes [IL-6, TNF-a, basic fibroblast growth factor (FGF) and eotaxin ]
Michielsen et al., PloS one 2011 (Colorectal Neoplasms) : Pre-treatment of monocyte derived dendritic cells with this tumour conditioned media inhibited the up-regulation of CD86 , CD83, CD54 and HLA-DR in response to LPS , enhancing IL-10 while reducing IL-12p70 secretion
Brake et al., Parasites & vectors 2012 (Cattle Diseases...) : At 24 hrs CD80, CD86 , and CD69 expression was increased with LPS , but was inhibited by the addition of SGE
Vilekar et al., Int Immunol 2012 : EF24 reduced the expression of LPS induced MHC class II, CD80 and CD86 molecules
Dangi et al., J Immunol 2012 : LPS increased the expression of MHC class II, CD80, and CD86 and stimulated the production of IL-1a, IL-1ß, IL-6, IL-10 and TNF-a by HSCs. Interestingly, production of IL-1a, IL-1ß, IL-6, and TNF-a was strongly inhibited, but that of IL-10 enhanced in LPS pretreated HSC/Treg cocultures
Tsukamoto et al., Int Immunol 2012 : HT52 and HT4 mAbs inhibited LPS induced nuclear factor-?B activation in TLR4/MD-2 expressing Ba/F3 transfected cells and cytokine production and up-regulation of CD86 in the human cell line U373 and PBMCs
Fu et al., PloS one 2013 (Inflammation) : The expression of LPS induced major histocompatibility complex class II, CD40, and CD86 on DCs was also decreased by acetylcorynoline, and the endocytic capacity of LPS stimulated DCs was restored by acetylcorynoline
Sung et al., Biochem Biophys Res Commun 2013 : Lipopolysaccharide (LPS) induced expression of cell surface molecules ( CD80, CD86 , and MHC class I/II ) and production of pro-inflammatory cytokines ( tumor necrosis factor-a, IL-1ß, IL-6, and IL-12p70 ) were inhibited by Pro B2, and this action was prevented by IRAK-M silencing
Jakob et al., J Immunol 1998 : Flow cytometry of FSDDC-A revealed that IL-1, TNF-alpha, and LPS induced increased expression of MHC class II, CD40, and CD86 and decreased E-cadherin expression that was temporally related to dissociation of aggregates