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IL12A — MYD88

Text-mined interactions from Literome

Seki et al., J Immunol 2001 : These results indicate that MyD88 is essential for IL-12 and IL-1beta production from Kupffer cells while their IL-18 secretion is mediated via activation of endogenous caspase-1 without de novo protein synthesis in a MyD88 independent fashion after stimulation with LPS
Seki et al., J Immunol 2002 (Inflammation...) : These results indicated a critical role for TLRs/MyD88 dependent IL-12/TNF-alpha production and for IL-12- and IL-18 mediated IFN-gamma production in early phase clearance of LM
Huang et al., J Immunol 2003 : Our results show that HKBA mediated induction of IL-12p40 and TNF is dependent on the adapter molecule MyD88
Bafica et al., J Immunol 2006 (Chagas Disease) : Our results reveal that TLR2 and TLR9 cooperate in the control of parasite replication and that TLR9 has a primary role in the MyD88 dependent induction of IL-12/IFN-gamma synthesis during infection with T. cruzi
Goodridge et al., Parasite Immunol 2007 : PC-Ova mimicked the modulation of interleukin (IL)-12 production by ES-62 in a TLR4- and MyD88 dependent manner and as with native ES-62, PC-Ova effects were not dependent on Pro712
Ichikawa et al., Biosci Biotechnol Biochem 2007 : MyD88 but not TLR2, 4 or 9 is essential for IL-12 induction by lactic acid bacteria
Yammani et al., Virology 2008 : Importantly, the control of IL-12 production was differentially dependent on MyD88 signaling
Durães et al., Immunol Lett 2009 : IL-12 and TNF-alpha production by dendritic cells stimulated with Schistosoma mansoni schistosomula tegument is TLR4- and MyD88 dependent
Langlet et al., Eur J Immunol 2010 : Unexpectedly, BM-derived DC from PKC-alpha ( -/- ) mice exhibited decreased TNF-alpha and IL-12p40 production induced by both MyD88- and TRIF dependent ligands
Krummen et al., J Leukoc Biol 2010 : Release of IL-12 by dendritic cells activated by TLR ligation is dependent on MyD88 signaling, whereas TRIF signaling is indispensable for TLR synergy
Chen et al., Biomaterials 2010 : The result that MyD88 inhibitor remarkably reduced the IL-12 expression induced by cationic polymers suggested that this stimulation was mainly mediated by toll-like receptor ( TLR ) pathway
Mendes et al., Vaccine 2011 (Toxoplasmosis, Animal) : We conclude that protective parasite specific-CD8 ( + ) T cells are elicited by a mechanism that involves MyD88 dependent induction of IL-12
Butcher et al., PLoS Pathog 2011 : High level IL-12p40 production in dROP16 infection was dependent on the host cell adaptor molecule MyD88 , but surprisingly was independent of any previously recognized T. gondii triggered pathway linking to MyD88 ( TLR2, TLR4, TLR9, TLR11, IL-1ß and IL-18 )
Goodyear et al., Infect Immun 2012 (Disease Models, Animal...) : Thus, we conclude that the MyD88 dependent recruitment of inflammatory monocytes and DCs to the lungs and the local production of IL-12 , followed by NK cell production of IFN-?, are the key initial cellular responses required for early protection from B. mallei infection
Zhang et al., Cell Mol Immunol 2012 : Brucella abortus is a Gram negative intracellular bacterium that induces MyD88 dependent IL-12 production in dentritic cells (DCs) and a subsequent protective Th1 immune response
Klaas et al., J Immunol 2012 : This was accompanied by a strong reduction in MyD88 dependent secretion of TNF-a, IL-6, IL-12 , and IL-10