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10.1073/pnas.1707840114 http://scihub22266oqcxt.onion/10.1073/pnas.1707840114 C5651758!5651758 !28973928     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28973928 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mycobacterium tuberculosis inhibits human innate immune responses via the production of TLR2 antagonist glycolipids |pdf=|usr=}}{{28973928 }} gab.com Text Mycobacterium tuberculosis inhibits human innate immune responses via the production of TLR2 antagonist glycolipids JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28973928 #FOAvip Mycobacterium tuberculosis is a major human pathogen that is able to survive inside host cells and resist immune clearance. Most particularly, it inhibits several arms of the innate immune response, including phagosome maturation or cytokine production. To better understand the molecular mechanisms by which M. tuberculosis circumvents host immune defenses, we used a transposon mutant library generated in a virulent clinical isolate of M. tuberculosis of the W/Beijing family to infect human macrophages, utilizing a cell line derivative of THP-1 cells expressing a reporter system for activation of the transcription factor NF-?B, a key regulator of innate immunity. We identified several M. tuberculosis mutants inducing a NF-?B activation stronger than that of the wild-type strain. One of these mutants was found to be deficient for the synthesis of cell envelope glycolipids, namely sulfoglycolipids, suggesting that the latter can interfere with innate immune responses. Using natural and synthetic molecular variants, we determined that sulfoglycolipids inhibit NF-?B activation and subsequent cytokine production or costimulatory molecule expression by acting as competitive antagonists of Toll-like receptor 2, thereby inhibiting the recognition of M. tuberculosis by this receptor. Our study reveals that producing glycolipid antagonists of pattern recognition receptors is a strategy used by M. tuberculosis to undermine innate immune defense. Sulfoglycolipids are major and specific lipids of M. tuberculosis, considered for decades as virulence factors of the bacilli. Our study uncovers a mechanism by which they may contribute to M. tuberculosis virulence. Twit Text FOAVip Mycobacterium tuberculosis inhibits human innate immune responses via the production of TLR2 antagonist glycolipids ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=28973928 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28973928 #FOAvip English Wikipedia <ref>{{Cite pmid|28973928 }}</ref> Mycobacterium tuberculosis inhibits human innate immune responses via the production of TLR2 antagonist glycolipids #MMPMID28973928 Blanc L ; Gilleron M ; Prandi J ; Song OR ; Jang MS ; Gicquel B ; Drocourt D ; Neyrolles O ; Brodin P ; Tiraby G ; Vercellone A ; Nigou J Proc Natl Acad Sci U S A 2017[Oct]; 114 (42 ): 11205-11210 PMID28973928 show ga Mycobacterium tuberculosis is a major human pathogen that is able to survive inside host cells and resist immune clearance. Most particularly, it inhibits several arms of the innate immune response, including phagosome maturation or cytokine production. To better understand the molecular mechanisms by which M. tuberculosis circumvents host immune defenses, we used a transposon mutant library generated in a virulent clinical isolate of M. tuberculosis of the W/Beijing family to infect human macrophages, utilizing a cell line derivative of THP-1 cells expressing a reporter system for activation of the transcription factor NF-?B, a key regulator of innate immunity. We identified several M. tuberculosis mutants inducing a NF-?B activation stronger than that of the wild-type strain. One of these mutants was found to be deficient for the synthesis of cell envelope glycolipids, namely sulfoglycolipids, suggesting that the latter can interfere with innate immune responses. Using natural and synthetic molecular variants, we determined that sulfoglycolipids inhibit NF-?B activation and subsequent cytokine production or costimulatory molecule expression by acting as competitive antagonists of Toll-like receptor 2, thereby inhibiting the recognition of M. tuberculosis by this receptor. Our study reveals that producing glycolipid antagonists of pattern recognition receptors is a strategy used by M. tuberculosis to undermine innate immune defense. Sulfoglycolipids are major and specific lipids of M. tuberculosis, considered for decades as virulence factors of the bacilli. Our study uncovers a mechanism by which they may contribute to M. tuberculosis virulence. |*Immunity, Innate [MESH] |Glycolipids/*metabolism/pharmacology [MESH] |Humans [MESH] |Macrophages/metabolism [MESH] |Mycobacterium tuberculosis/genetics/immunology/*metabolism [MESH] |NF-kappa B/metabolism [MESH]Mycobacterium tuberculosis inhibits human innate immune responses via (epmc).pdf DeepDyve Pubget Overpricing