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Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance
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Woods A Monneaux F Soulas-Sprauel P Muller S Martin T Korganow AS Pasquali JL 《Journal of virology》2007,81(22):12525-12534
The link between infection and autoimmunity is not yet well understood. This study was designed to evaluate if an acute viral infection known to induce type I interferon production, like influenza, can by itself be responsible for the breakdown of immune tolerance and for autoimmunity. We first tested the effects of influenza virus on B cells in vitro. We then infected different transgenic mice expressing human rheumatoid factors (RF) in the absence or in the constitutive presence of the autoantigen (human immunoglobulin G [IgG]) and young lupus-prone mice [(NZB x NZW)F(1)] with influenza virus and looked for B-cell activation. In vitro, the virus induces B-cell activation through type I interferon production by non-B cells but does not directly stimulate purified B cells. In vivo, both RF and non-RF B cells were activated in an autoantigen-independent manner. This activation was abortive since IgM and IgM-RF production levels were not increased in infected mice compared to uninfected controls, whether or not anti-influenza virus human IgG was detected and even after viral rechallenge. As in RF transgenic mice, acute viral infection of (NZB x NZW)F(1) mice induced only an abortive activation of B cells and no increase in autoantibody production compared to uninfected animals. Taken together, these experiments show that virus-induced acute type I interferon production is not able by itself to break down B-cell tolerance in both normal and autoimmune genetic backgrounds. 相似文献
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Christian Demeure Olivier Dussurget Guillem Mas Fiol Anne-Sophie Le Guern Cyril Savin Javier Pizarro-Cerdá 《Microbes and infection / Institut Pasteur》2019,21(5-6):202-212
Plague is a vector-borne disease caused by Yersinia pestis. Transmitted by fleas from rodent reservoirs, Y. pestis emerged less than 6000 years ago from an enteric bacterial ancestor through events of gene gain and genome reduction. It is a highly remarkable model for the understanding of pathogenic bacteria evolution, and a major concern for public health as highlighted by recent human outbreaks. A complex set of virulence determinants, including the Yersinia outer membrane proteins (Yops), the broad range protease Pla, pathogen-associated molecular patterns (PAMPs) and iron capture systems play critical roles in the molecular strategies that Y. pestis employs to subvert the human immune system, allowing unrestricted bacterial replication in lymph nodes (bubonic plague) and in lungs (pneumonic plague). Some of these immunogenic proteins as well as the capsular antigen F1 are exploited for diagnostic purposes, which are critical in the context of the rapid onset of death in the absence of antibiotic treatment (less than a week for bubonic plague and less than 48 h for pneumonic plague). In here, we review recent research advances on Y. pestis evolution, virulence factors function, bacterial strategies to subvert mammalian innate immune responses, vaccination and problems associated to pneumonic plague diagnosis. 相似文献
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Céline Crauste Nicolas Willand Baptiste Villemagne Marion Flipo Eve Willery Xavier Carette Martin Moune Dimala Anne-Sophie Drucbert Pierre-Marie Danze Benoit Deprez Alain R. Baulard 《Analytical biochemistry》2014
EthR is a mycobacterial repressor that limits the bioactivation of ethionamide, a commonly used anti-tuberculosis second-line drug. Several efforts have been deployed to identify EthR inhibitors abolishing the DNA-binding activity of the repressor. This led to the demonstration that stimulating the bioactivation of Eth through EthR inhibition could be an alternative way to fight Mycobacterium tuberculosis. We propose a new surface plasmon resonance (SPR) methodology to study the affinity between inhibitors and EthR. Interestingly, the binding between inhibitors and immobilized EthR produced a dose-dependent negative SPR signal. We demonstrate that this signal reveals the affinity of small molecules for the repressor. The affinity constants (KD) correlate with their capacity to inhibit the binding of EthR to DNA. We hypothesize that conformational changes in EthR during ligand interaction could be responsible for this SPR signal. Practically, this unconventional result opens perspectives onto the development of an SPR assay that would at the same time reveal structural changes in the target upon binding with an inhibitor and the binding constant of this interaction. 相似文献
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Anne-Sophie Schillinger Cédric Grauffel Hanif Muhammad Khan Øyvind Halskau Nathalie Reuter 《生物化学与生物物理学报:生物膜》2014
Neutrophil serine proteases Proteinase 3 (PR3) and human neutrophil elastase (HNE) are homologous antibiotic serine proteases of the polymorphonuclear neutrophils. Despite sharing a 56% sequence identity they have been shown to have different functions and localizations in the neutrophils. In particular, and in contrast to HNE, PR3 has been detected at the outer leaflet of the plasma membrane and its membrane expression is a risk factor in a number of chronic inflammatory diseases. Although a plethora of studies performed in various cell-based assays have been reported, the mechanism by which PR3, and possibly HNE bind to simple membrane models remains unclear. We used surface plasmon resonance (SPR) experiments to measure and compare the affinity of PR3 and HNE for large unilamellar vesicles composed of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC). We also conducted 500-nanosecond long molecular dynamics simulations of each enzyme at the surface of a POPC bilayer to map the interactions between proteins and lipids and rationalize the difference in affinity observed in the SPR experiment. We find that PR3 binds strongly to POPC large unilamellar vesicles (Kd = 9.2 × 10− 7 M) thanks to the insertion of three phenylalanines, one tryptophan and one leucine beyond the phosphate groups of the POPC lipids. HNE binds in a significantly weaker manner (Kd > 10− 5 M) making mostly electrostatic interactions via lysines and arginines and inserting only one leucine between the hydrophobic lipid tails. Our results support the early reports that PR3, unlike HNE, is able to directly and strongly anchor directly to the neutrophil membrane. 相似文献
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Laurence Wurth Anne-Sophie Gribling-Burrer Céline Verheggen Michael Leichter Akiko Takeuchi Stéphanie Baudrey Franck Martin Alain Krol Edouard Bertrand Christine Allmang 《Nucleic acids research》2014,42(13):8663-8677
Mammalian mRNAs are generated by complex and coordinated biogenesis pathways and acquire 5′-end m7G caps that play fundamental roles in processing and translation. Here we show that several selenoprotein mRNAs are not recognized efficiently by translation initiation factor eIF4E because they bear a hypermethylated cap. This cap modification is acquired via a 5′-end maturation pathway similar to that of the small nucle(ol)ar RNAs (sn- and snoRNAs). Our findings also establish that the trimethylguanosine synthase 1 (Tgs1) interacts with selenoprotein mRNAs for cap hypermethylation and that assembly chaperones and core proteins devoted to sn- and snoRNP maturation contribute to recruiting Tgs1 to selenoprotein mRNPs. We further demonstrate that the hypermethylated-capped selenoprotein mRNAs localize to the cytoplasm, are associated with polysomes and thus translated. Moreover, we found that the activity of Tgs1, but not of eIF4E, is required for the synthesis of the GPx1 selenoprotein in vivo. 相似文献
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Manuela Ruiz Diaz Britez Anne-Sophie Sergent Alejandro Martinez Meier Nathalie Bréda Philippe Rozenberg 《Trees - Structure and Function》2014,28(5):1289-1304
Key message
Proxies of adaptive traits for resistance to drought were discovered among original annual ring density variables in Douglas fir.Abstract
A comparison of dead and surviving Douglas fir trees following the 2003 drought was made to define proxies of adaptive traits for resistance to drought. Increment cores were sampled from trees from three French regions: Centre, Midi-Pyrénées and Burgundy. Original tree-ring variables were calculated, based on a sliding density criterion dividing the microdensity profile into high- and low-density segments. Tree rings were analysed at each site in a number of consecutive annual rings before the 2003 drought event. Comparison between pairs of surviving and dead trees and between pairs of randomly selected trees (whether dead or alive) supports the evidence of systematic dissimilarities between surviving and dead trees in a number of original density variables. Correlation analysis between original and conventional ring density variables indicates a weak association. We found that the surviving trees were denser than the dead trees in all three sites, but that the denser part of the ring varied from region to region. We identified several original density variables intended to be used as proxies of adaptive traits in future studies of genetic determinism of Douglas fir resistance to drought. 相似文献139.
Fabrice Legeai Sylvie Gimenez Bernard Duvic Jean-Michel Escoubas Anne-Sophie Gosselin Grenet Florence Blanc Fran?ois Cousserans Imène Séninet Anthony Bretaudeau Doriane Mutuel Pierre-Alain Girard Christelle Monsempes Ghislaine Magdelenat Frédérique Hilliou René Feyereisen Mylène Ogliastro Anne-Nathalie Volkoff Emmanuelle Jacquin-Joly Emmanuelle d’Alen?on Nicolas Nègre Philippe Fournier 《BMC genomics》2014,15(1)
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Rigmor Thorstensson Birger Trollfors Nabil Al-Tawil Maja Jahnmatz Jakob Bergstr?m Margaretha Ljungman Anna T?rner Lena Wehlin Annie Van Broekhoven Fons Bosman Anne-Sophie Debrie Nathalie Mielcarek Camille Locht 《PloS one》2014,9(1)