IndraLab

Statements

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"Mechanistically , HCQ down-regulated the expression of TLR9 not only in healthy donor PBMC-derived DCs stimulated by RA patient serum , but also in LN DCs of CIA mice and CpG-activated BMDCs ."
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"In addition , hydroxychloroquine ( HCQ ) and ODN2088 were used to inhibit TLR9 to investigate the role of TLR9 on caspase3 / GSDME-mediated pyroptosis ."
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"The mechanism of the inhibition of endosomal TLR 7 and TLR9 by HCQ and CQ has been presented in Fig."
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"Given that the endosomal maturation inhibitor hydroxychloroquine inhibits TLR9 activation and is a common treatment for SjS XREF_BIBR, we injected NOD and BALB/c mice with ODN2088, which dramatically increased salivation in NOD mice (p = 0.0018) (XREF_FIG)."
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"Nonetheless, given the proposed mechanism of action via TLR9, it seems possible that hydroxychloroquine and chloroquine might prevent the activation of nucleic acid sensors cGAS and TLR9 through a common mechanism such as alteration of the structural configuration of the DNA substrate [33,34]."
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"Again, HCQ prevented the upregulation of TLR9 as anticipated."
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"Again, HCQ prevented the up-regulation of TLR9 as anticipated (XREF_FIG B)."
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"On the contrary, Yu et al., have hypothesized that hydroxychloroquine and other antimalarials, by inhibiting the toll like receptor-9 (TLR9), may induce persistence of HPV in lupus erythematosus patients."
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"Taken together, hydroxychloroquine markedly suppresses the TLR9 mediated human B cell functions during inflammatory processes."
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"In antigen-presenting cells, HCQ also reduced constitutive activation of the endo-lysosomal protease legumain and toll-like receptor 9, thereby reducing cytokine production, but it had little apparent impact on constitutive antigen processing and peptide presentation."
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"We supposed that the reasons are as follows : ( 1 ) the immune regulation function of HCQ in suppressing the secretion of pro-inflammatory factors [ 11,12 ] , which can be explained by our results that HCQ diminished the levels of pro-inflammatory factors including IFN-alpha , TNF-alpha , IL-1beta and IL-12 by blocking TLR9 ; ( 2 ) however , as mentioned above , HCQ could only blocking TLR9 , so it just partially reduces the production of inflammatory cytokines ."
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"In rheumatoid arthritis and systemic lupus erythematosus, hydroxychloroquine has been suggested to mediate its anti-inflammatory action by inhibiting the activation of TLR7 and TLR9 that reside in endosomal/lysosomal compartments 23."
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"The TLR7 to TLR9 blocker hydroxychloroquine has been in use in patients with lupus for more than 50years, but oligonucleotide based inhibitors of TLR7 to TLR9, despite showing promise in animal models of lupus, have not reached the primary end point in a recent phase 1 trial."
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"Indeed, in vivo treatment with HCQ in SLE patients has been shown to inhibit TLR7 and TLR9-dependent activation of pDCs upon ex vivo exposure of pDCs with specific TLR ligands [24] ."
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"Other Toll-like targets are of interest as well, such as TLR-7 and TLR-9 blockage by hydroxychloroquine, which has been used successfully in inflammatory disorders such as systemic lupus erythematosus [52] and post-Lyme’s arthritis [53]."
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"In addition, hydroxychloroquine (HCQ) and ODN2088 were used to inhibit TLR9 to investigate the role of TLR9 on caspase3/GSDME-mediated pyroptosis."
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"Hydroxychloroquine blocks TLR9 activation by mitochondrial DNA in vitro and may attenuate flares of rhabdomyolysis in 6 patients treated."
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"Again , HCQ prevented the up-regulation of TLR9 as anticipated ( Fig. 4B ) ."
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"The mechanism of the inhibition of endosomal TLR 7 and TLR9 by HCQ and CQ has been presented in Fig. 5 [ 58 ] ."
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"Hydroxychloroquine works by inhibiting the binding of TLR9 to the ligand CPG-DNA so that TLR9 cannot be activated (Rutz et al., 2004)."
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"Hydroxychloroquine is a potent inhibitor of TLR-9, and to a lesser extent TLR-7 and TLR-8, and inhibits antigen processing and presentation via alkalinization of proteasomes [XREF_BIBR, XREF_BIBR]."
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"A role of TLRs in HIV induced immune activation is also supported by the reduction in immune activation by TLR7 and TLR9 signaling inhibitors such as chloroquine and hydroxychloroquine [XREF_BIBR, XREF_BIBR]."
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"HCQ blocking TLR9 protects against hepatic I/R injury by inhibiting NETs formation, which may suggest utility of HCQ or other TLR9 agonists for preventing hepatic I/R injury in clinical practices."
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"Since hydroxychloroquine and chloroquine are inhibitors of the anti-viral PRRs TLR9 and cGAS, they may provide a means of improving AAV transduction by modulating anti-viral responses during gene therapy."
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