The D-helix peptide 2R9 also potently inhibited TLR4 TLR7 and TLR9 but not TLR3 or TNF-alpha signaling. Cell imaging co-immunoprecipitation and in vitro studies demonstrated that 2R9 preferentially targets TIRAP.
DC activation induced by TLR3 -4 -7 and -9 ligands also augments Trex1 expression through autocrine IFN-beta production and triggering of the IFN signaling pathway
Our findings indicate that TLR7 plays a central role in early immune activation during malaria infection whereas TLR7 and TLR9 contribute combinatorially to immune responses as infection progresses.
TLR2 inhibits IFN-I induction by TLR7/9 may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9 or responses to bacteria/virus coinfection.
Studies identify agonists of TLR3 TLR4 TLR7 and particularly agonist of TLR9 as the best adjuvants for the induction of antigen-specific CD4+ T-cell effectors.
A pivotal role for phagolysosomal TLR7 signaling in fungal pathogen recognition also highlights the importance of type I interferons (IFNs-I) in modulating the host immune response to Candida glabrata.
Studies demonstrate that macrophages lacking TLR3 TRIF TLR7 or TLR9 individually or both TLR4 and MyD88 still induce IFN-beta equivalent to wild type controls leading to the hypothesis that TLR-independent pathways are crucial for this response.
These results demonstrate previously unknown crucial regulatory mechanisms that alter ARR/GRK expression levels in macrophages that might modify many if not all GPCR-mediated innate immune responses.
Results suggest novel signaling pathway in murine macrophages involving synergy between toll-like receptors 2 4 7 and 9 and adenosine A(2A)receptors that up-regulates VEGF and down-regulates TNFalpha expression thus acting as an angiogenic switch.
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