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10.1038/srep44042

http://scihub22266oqcxt.onion/10.1038/srep44042
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C5339793!5339793!28266597
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suck abstract from ncbi


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pmid28266597      Sci+Rep 2017 ; 7 (ä): ä
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  • The protective effect of the anti-Toll-like receptor 9 antibody against acute cytokine storm caused by immunostimulatory DNA #MMPMID28266597
  • Murakami Y; Fukui R; Motoi Y; Shibata T; Saitoh SI; Sato R; Miyake K
  • Sci Rep 2017[]; 7 (ä): ä PMID28266597show ga
  • Toll-like Receptor 9 (TLR9) is an innate immune receptor recognizing microbial DNA. TLR9 is also activated by self-derived DNA, such as mitochondrial DNA, in a variety of inflammatory diseases. We show here that TLR9 activation in vivo is controlled by an anti-TLR9 monoclonal Ab (mAb). A newly established mAb, named NaR9, clearly detects endogenous TLR9 expressed in primary immune cells. The mAb inhibited TLR9-dependent cytokine production in vitro by bone marrow-derived macrophages and conventional dendritic cells. Furthermore, NaR9 treatment rescued mice from fulminant hepatitis caused by administering the TLR9 ligand CpGB and D-(+)-galactosamine. The production of proinflammatory cytokines induced by CpGB and D-(+)-galactosamine was significantly impaired by the mAb. These results suggest that a mAb is a promising tool for therapeutic intervention in TLR9-dependent inflammatory diseases.
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