-
Something wrong with this record ?
Subversion of innate immune responses by Francisella involves the disruption of TRAF3 and TRAF6 signalling complexes
D. Putzova, S. Panda, A. Härtlova, J. Stulík, NO. Gekara,
Language English Country England, Great Britain
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Free Medical Journals
from 1999 to 2 years ago
Medline Complete (EBSCOhost)
from 1999-07-01 to 2021-12-31
Wiley Free Content
from 1999 to 2021
ROAD: Directory of Open Access Scholarly Resources
from 1999
PubMed
28745813
DOI
10.1111/cmi.12769
Knihovny.cz E-resources
- MeSH
- Adaptor Proteins, Signal Transducing genetics MeSH
- Adaptor Proteins, Vesicular Transport genetics MeSH
- TNF Receptor-Associated Factor 3 metabolism MeSH
- TNF Receptor-Associated Factor 6 metabolism MeSH
- Francisella tularensis immunology pathogenicity MeSH
- Immune Evasion immunology MeSH
- Myeloid Differentiation Factor 88 genetics MeSH
- Mice, Inbred C57BL MeSH
- Mice, Knockout MeSH
- Mice MeSH
- Immunity, Innate immunology MeSH
- Receptors, Pattern Recognition antagonists & inhibitors MeSH
- Type VI Secretion Systems metabolism MeSH
- Tularemia immunology microbiology pathology MeSH
- Ubiquitination immunology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
The success of pathogens depends on their ability to circumvent immune defences. Francisella tularensis is one of the most infectious bacteria known. The remarkable virulence of Francisella is believed to be due to its capacity to evade or subvert the immune system, but how remains obscure. Here, we show that Francisella triggers but concomitantly inhibits the Toll-like receptor, RIG-I-like receptor, and cytoplasmic DNA pathways. Francisella subverts these pathways at least in part by inhibiting K63-linked polyubiquitination and assembly of TRAF6 and TRAF3 complexes that control the transcriptional responses of pattern recognition receptors. We show that this mode of inhibition requires a functional type VI secretion system and/or the presence of live bacteria in the cytoplasm. The ability of Francisella to enter the cytosol while simultaneously inhibiting multiple pattern recognition receptor pathways may account for the notable capacity of this bacterium to invade and proliferate in the host without evoking a self-limiting innate immune response.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc18033807
- 003
- CZ-PrNML
- 005
- 20181023105445.0
- 007
- ta
- 008
- 181008s2017 enk f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1111/cmi.12769 $2 doi
- 035 __
- $a (PubMed)28745813
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a enk
- 100 1_
- $a Putzova, Daniela $u Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden. Department of Molecular Pathology and Biology, Faculty of Military Health Sciences, University of Defense, Hradec Králové, Czech Republic.
- 245 10
- $a Subversion of innate immune responses by Francisella involves the disruption of TRAF3 and TRAF6 signalling complexes / $c D. Putzova, S. Panda, A. Härtlova, J. Stulík, NO. Gekara,
- 520 9_
- $a The success of pathogens depends on their ability to circumvent immune defences. Francisella tularensis is one of the most infectious bacteria known. The remarkable virulence of Francisella is believed to be due to its capacity to evade or subvert the immune system, but how remains obscure. Here, we show that Francisella triggers but concomitantly inhibits the Toll-like receptor, RIG-I-like receptor, and cytoplasmic DNA pathways. Francisella subverts these pathways at least in part by inhibiting K63-linked polyubiquitination and assembly of TRAF6 and TRAF3 complexes that control the transcriptional responses of pattern recognition receptors. We show that this mode of inhibition requires a functional type VI secretion system and/or the presence of live bacteria in the cytoplasm. The ability of Francisella to enter the cytosol while simultaneously inhibiting multiple pattern recognition receptor pathways may account for the notable capacity of this bacterium to invade and proliferate in the host without evoking a self-limiting innate immune response.
- 650 _2
- $a adaptorové proteiny signální transdukční $x genetika $7 D048868
- 650 _2
- $a adaptorové proteiny vezikulární transportní $x genetika $7 D033942
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a Francisella tularensis $x imunologie $x patogenita $7 D005604
- 650 _2
- $a imunitní únik $x imunologie $7 D057131
- 650 _2
- $a přirozená imunita $x imunologie $7 D007113
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a myši inbrední C57BL $7 D008810
- 650 _2
- $a myši knockoutované $7 D018345
- 650 _2
- $a myeloidní diferenciační faktor 88 $x genetika $7 D053594
- 650 _2
- $a receptory rozpoznávající vzory $x antagonisté a inhibitory $7 D051192
- 650 _2
- $a faktor 3 asociovaný s receptory TNF $x metabolismus $7 D048008
- 650 _2
- $a faktor 6 asociovaný s receptory TNF $x metabolismus $7 D048029
- 650 _2
- $a tularemie $x imunologie $x mikrobiologie $x patologie $7 D014406
- 650 _2
- $a sekreční systém typu VI $x metabolismus $7 D000069376
- 650 _2
- $a ubikvitinace $x imunologie $7 D054875
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Panda, Swarupa $u Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
- 700 1_
- $a Härtlova, Anetta $u Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
- 700 1_
- $a Stulík, Jiří $u Department of Molecular Pathology and Biology, Faculty of Military Health Sciences, University of Defense, Hradec Králové, Czech Republic.
- 700 1_
- $a Gekara, Nelson O $u Department of Molecular Biology, The Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
- 773 0_
- $w MED00007154 $t Cellular microbiology $x 1462-5822 $g Roč. 19, č. 11 (2017)
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/28745813 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20181008 $b ABA008
- 991 __
- $a 20181023105952 $b ABA008
- 999 __
- $a ok $b bmc $g 1340305 $s 1030801
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2017 $b 19 $c 11 $e 20170816 $i 1462-5822 $m Cellular microbiology $n Cell Microbiol $x MED00007154
- LZP __
- $a Pubmed-20181008