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19 results on '"Gardet, Agnes"'

4. Genetics and pathogenesis of inflammatory bowel disease

Author

Khor, Bernard, Gardet, Agnes, and Xavier, Ramnik J.

Subjects
Inflammatory bowel diseases -- Development and progression -- Genetic aspects, Immune system -- Genetic aspects -- Health aspects, Host-bacteria relationships -- Genetic aspects -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Recent advances have provided substantial insight into the maintenance of mucosal immunity and the pathogenesis of inflammatory bowel disease. Cellular programs responsible for intestinal homeostasis use diverse intracellular and intercellular networks to promote immune tolerance, inflammation or epithelial restitution. Complex interfaces integrate local host and microbial signals to activate appropriate effector programs selectively and even drive plasticity between these programs. In addition, genetic studies and mouse models have emphasized the role of genetic predispositions and how they affect interactions with microbial and environmental factors, leading to pro-colitogenic perturbations of the host-commensal relationship., Author(s): Bernard Khor [sup.1] [sup.2] [sup.3] , Agnès Gardet [sup.1] [sup.2] , Ramnik J. Xavier [sup.1] [sup.2] [sup.4] Author Affiliations: (1) Gastrointestinal Unit and Center for the Study of Inflammatory [...]

Published
2011
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8. Monoclonal antibody targeting BDCA2 ameliorates skin lesions in systemic lupus erythematosus

Author

Furie, Richard, primary, Werth, Victoria P., additional, Merola, Joseph F., additional, Stevenson, Lauren, additional, Reynolds, Taylor L., additional, Naik, Himanshu, additional, Wang, Wenting, additional, Christmann, Romy, additional, Gardet, Agnes, additional, Pellerin, Alex, additional, Hamann, Stefan, additional, Auluck, Pavan, additional, Barbey, Catherine, additional, Gulati, Parul, additional, Rabah, Dania, additional, and Franchimont, Nathalie, additional

Published
2019
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10. Pristane-Accelerated Autoimmune Disease in (SWR X NZB) F1 Mice Leads to Prominent Tubulointerstitial Inflammation and Human Lupus Nephritis-Like Fibrosis

Author

Gardet, Agnes, primary, Chou, Wei C., additional, Reynolds, Taylor L., additional, Velez, Diana B., additional, Fu, Kai, additional, Czerkowicz, Julia M., additional, Bajko, Jeffrey, additional, Ranger, Ann M., additional, Allaire, Normand, additional, Kerns, Hannah M., additional, Ryan, Sarah, additional, Legault, Holly M., additional, Dunstan, Robert W., additional, Lafyatis, Robert, additional, Lukashev, Matvey, additional, Viney, Joanne L., additional, Browning, Jeffrey L., additional, and Rabah, Dania, additional

Published
2016
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12. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease

Author

Rivas, Manuel A., Beaudoin, Melissa, Gardet, Agnes, Stevens, Christine, Sharma, Yashoda, Zhang, Clarence K., Boucher, Gabrielle, Ripke, Stephan, Ellinghaus, David, Burtt, Noel, Fennell, Tim, Kirby, Andrew, Latiano, Anna, Goyette, Philippe, Green, Todd, Halfvarson, Jonas, Haritunians, Talin, Korn, Joshua M., Kuruvilla, Finny, Lagace, Caroline, Neale, Benjamin, Lo, Ken Sin, Schumm, Phil, Torkvist, Leif, Dubinsky, Marla C., Brant, Steven R., Silverberg, Mark S., Duerr, Richard H., Altshuler, David, Gabriel, Stacey, Lettre, Guillaume, Franke, Andre, D'Amato, Mauro, McGovern, Dermot P. B., Cho, Judy H., Rioux, John D., Xavier, Ramnik J., Daly, Mark J., Rivas, Manuel A., Beaudoin, Melissa, Gardet, Agnes, Stevens, Christine, Sharma, Yashoda, Zhang, Clarence K., Boucher, Gabrielle, Ripke, Stephan, Ellinghaus, David, Burtt, Noel, Fennell, Tim, Kirby, Andrew, Latiano, Anna, Goyette, Philippe, Green, Todd, Halfvarson, Jonas, Haritunians, Talin, Korn, Joshua M., Kuruvilla, Finny, Lagace, Caroline, Neale, Benjamin, Lo, Ken Sin, Schumm, Phil, Torkvist, Leif, Dubinsky, Marla C., Brant, Steven R., Silverberg, Mark S., Duerr, Richard H., Altshuler, David, Gabriel, Stacey, Lettre, Guillaume, Franke, Andre, D'Amato, Mauro, McGovern, Dermot P. B., Cho, Judy H., Rioux, John D., Xavier, Ramnik J., and Daly, Mark J.

Abstract

More than 1,000 susceptibility loci have been identified through genome-wide association studies (GWAS) of common variants; however, the specific genes and full allelic spectrum of causal variants underlying these findings have not yet been defined. Here we used pooled next-generation sequencing to study 56 genes from regions associated with Crohn's disease in 350 cases and 350 controls. Through follow-up genotyping of 70 rare and low-frequency protein-altering variants in nine independent case-control series (16,054 Crohn's disease cases, 12,153 ulcerative colitis cases and 17,575 healthy controls), we identified four additional independent risk factors in NOD2, two additional protective variants in IL23R, a highly significant association with a protective splice variant in CARD9 (P < 1 x 10(-16), odds ratio approximate to 0.29) and additional associations with coding variants in IL18RAP, CUL2, C1orf106, PTPN22 and MUC19. We extend the results of successful GWAS by identifying new, rare and probably functional variants that could aid functional experiments and predictive models.

Published
2011
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13. Genome-wide association identifies multiple ulcerative colitis susceptibility loci (vol 42, pg 332, 2010)

Author

McGovern, Dermot P. B., Gardet, Agnes, Törkvist, Leif, Goyette, Philippe, Essers, Jonah, Taylor, Kent D., Neale, Benjamin M., Ong, Rick T. H., Lagace, Caroline, Li, Chun, Green, Todd, Stevens, Christine R., Beauchamp, Claudine, Fleshner, Phillip R., Carlson, Marie, D'Amato, Mauro, Halfvarson, Jonas, Hibberd, Martin L., Loerdal, Mikael, Padyukov, Leonid, Andriulli, Angelo, Colombo, Elisabetta, Latiano, Anna, Palmieri, Orazio, Bernard, Edmond-Jean, Deslandres, Colette, Hommes, Daan W., de Jong, Dirk J., Stokkers, Pieter C., Weersma, Rinse K., Sharma, Yashoda, Silverberg, Mark S., Cho, Judy H., Wu, Jing, Roeder, Kathryn, Brant, Steven R., Schumm, L. Phillip, Duerr, Richard H., Dubinsky, Marla C., Glazer, Nicole L., Haritunians, Talin, Ippoliti, Andy, Melmed, Gil Y., Siscovick, David S., Vasiliauskas, Eric A., Targan, Stephan R., Annese, Vito, Wijmenga, Cisca, Pettersson, Sven, Rotter, Jerome I., Xavier, Ramnik J., Daly, Mark J., Rioux, John D., Seielstad, Mark, McGovern, Dermot P. B., Gardet, Agnes, Törkvist, Leif, Goyette, Philippe, Essers, Jonah, Taylor, Kent D., Neale, Benjamin M., Ong, Rick T. H., Lagace, Caroline, Li, Chun, Green, Todd, Stevens, Christine R., Beauchamp, Claudine, Fleshner, Phillip R., Carlson, Marie, D'Amato, Mauro, Halfvarson, Jonas, Hibberd, Martin L., Loerdal, Mikael, Padyukov, Leonid, Andriulli, Angelo, Colombo, Elisabetta, Latiano, Anna, Palmieri, Orazio, Bernard, Edmond-Jean, Deslandres, Colette, Hommes, Daan W., de Jong, Dirk J., Stokkers, Pieter C., Weersma, Rinse K., Sharma, Yashoda, Silverberg, Mark S., Cho, Judy H., Wu, Jing, Roeder, Kathryn, Brant, Steven R., Schumm, L. Phillip, Duerr, Richard H., Dubinsky, Marla C., Glazer, Nicole L., Haritunians, Talin, Ippoliti, Andy, Melmed, Gil Y., Siscovick, David S., Vasiliauskas, Eric A., Targan, Stephan R., Annese, Vito, Wijmenga, Cisca, Pettersson, Sven, Rotter, Jerome I., Xavier, Ramnik J., Daly, Mark J., Rioux, John D., and Seielstad, Mark

Published
2011
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14. Genome-wide association identifies multiple ulcerative colitis susceptibility loci

Author

McGovern, Dermot P. B., Gardet, Agnes, Torkvist, Leif, Goyette, Philippe, Essers, Jonah, Taylor, Kent D., Neale, Benjamin M., Ong, Rick T. H., Lagace, Caroline, Li, Chun, Green, Todd, Stevens, Christine R., Beauchamp, Claudine, Fleshner, Phillip R., Carlson, Marie, D'Amato, Mauro, Halfvarson, Jonas, Hibberd, Martin L., Lordal, Mikael, Padyukov, Leonid, Andriulli, Angelo, Colombo, Elisabetta, Latiano, Anna, Palmieri, Orazio, Bernard, Edmond-Jean, Deslandres, Colette, Hommes, Daan W., de Jong, Dirk J., Stokkers, Pieter C., Weersma, Rinse K., Sharma, Yashoda, Silverberg, Mark S., Cho, Judy H., Wu, Jing, Roeder, Kathryn, Brant, Steven R., Schumm, L. Phillip, Duerr, Richard H., Dubinsky, Marla C., Glazer, Nicole L., Haritunians, Talin, Ippoliti, Andy, Melmed, Gil Y., Siscovick, David S., Vasiliauskas, Eric A., Targan, Stephan R., Annese, Vito, Wijmenga, Cisca, Pettersson, Sven, Rotter, Jerome I., Xavier, Ramnik J., Daly, Mark J., Rioux, John D., Seielstad, Mark, McGovern, Dermot P. B., Gardet, Agnes, Torkvist, Leif, Goyette, Philippe, Essers, Jonah, Taylor, Kent D., Neale, Benjamin M., Ong, Rick T. H., Lagace, Caroline, Li, Chun, Green, Todd, Stevens, Christine R., Beauchamp, Claudine, Fleshner, Phillip R., Carlson, Marie, D'Amato, Mauro, Halfvarson, Jonas, Hibberd, Martin L., Lordal, Mikael, Padyukov, Leonid, Andriulli, Angelo, Colombo, Elisabetta, Latiano, Anna, Palmieri, Orazio, Bernard, Edmond-Jean, Deslandres, Colette, Hommes, Daan W., de Jong, Dirk J., Stokkers, Pieter C., Weersma, Rinse K., Sharma, Yashoda, Silverberg, Mark S., Cho, Judy H., Wu, Jing, Roeder, Kathryn, Brant, Steven R., Schumm, L. Phillip, Duerr, Richard H., Dubinsky, Marla C., Glazer, Nicole L., Haritunians, Talin, Ippoliti, Andy, Melmed, Gil Y., Siscovick, David S., Vasiliauskas, Eric A., Targan, Stephan R., Annese, Vito, Wijmenga, Cisca, Pettersson, Sven, Rotter, Jerome I., Xavier, Ramnik J., Daly, Mark J., Rioux, John D., and Seielstad, Mark

Abstract

Ulcerative colitis is a chronic, relapsing inflammatory condition of the gastrointestinal tract with a complex genetic and environmental etiology. In an effort to identify genetic variation underlying ulcerative colitis risk, we present two distinct genome-wide association studies of ulcerative colitis and their joint analysis with a previously published scan(1), comprising, in aggregate, 2,693 individuals with ulcerative colitis and 6,791 control subjects. Fifty-nine SNPs from 14 independent loci attained an association significance of P < 10(-5). Seven of these loci exceeded genome-wide significance (P < 5 x 10(-8)). After testing an independent cohort of 2,009 cases of ulcerative colitis and 1,580 controls, we identified 13 loci that were significantly associated with ulcerative colitis (P < 5 x 10(-8)), including the immunoglobulin receptor gene FCGR2A, 5p15, 2p16 and ORMDL3 (orosomucoid1-like 3). We confirmed association with 14 previously identified ulcerative colitis susceptibility loci, and an analysis of acknowledged Crohn's disease loci showed that roughly half of the known Crohn's disease associations are shared with ulcerative colitis. These data implicate approximately 30 loci in ulcerative colitis, thereby providing insight into disease pathogenesis.

Published
2010
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18. Deep resequencing of GWAS loci identifies independent rare variants associated with inflammatory bowel disease.

Author

Rivas, Manuel A, Beaudoin, Mélissa, Gardet, Agnes, Stevens, Christine, Sharma, Yashoda, Zhang, Clarence K, Boucher, Gabrielle, Ripke, Stephan, Ellinghaus, David, Burtt, Noel, Fennell, Tim, Kirby, Andrew, Latiano, Anna, Goyette, Philippe, Green, Todd, Halfvarson, Jonas, Haritunians, Talin, Korn, Joshua M, Kuruvilla, Finny, and Lagacé, Caroline

Subjects
INFLAMMATORY bowel diseases, GENOMICS, GENOMES, CROHN'S disease, ULCERATIVE colitis, GENETICS
Abstract

More than 1,000 susceptibility loci have been identified through genome-wide association studies (GWAS) of common variants; however, the specific genes and full allelic spectrum of causal variants underlying these findings have not yet been defined. Here we used pooled next-generation sequencing to study 56 genes from regions associated with Crohn's disease in 350 cases and 350 controls. Through follow-up genotyping of 70 rare and low-frequency protein-altering variants in nine independent case-control series (16,054 Crohn's disease cases, 12,153 ulcerative colitis cases and 17,575 healthy controls), we identified four additional independent risk factors in NOD2, two additional protective variants in IL23R, a highly significant association with a protective splice variant in CARD9 (P < 1 × 10?16, odds ratio ? 0.29) and additional associations with coding variants in IL18RAP, CUL2, C1orf106, PTPN22 and MUC19. We extend the results of successful GWAS by identifying new, rare and probably functional variants that could aid functional experiments and predictive models. [ABSTRACT FROM AUTHOR]

Published
2011
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19. The C Terminus of Rotavirus VP4 Protein Contains an Actin Binding Domain Which Requires Cooperation with the Coiled-Coil Domain for Actin Remodeling.

Author

Condemine W, Eguether T, Couroussé N, Etchebest C, Gardet A, Trugnan G, and Chwetzoff S

Subjects
Animals, Binding Sites, COS Cells, Capsid Proteins genetics, Cell Line, Chlorocebus aethiops, Microscopy, Confocal, Microscopy, Fluorescence, Mutation, Protein Binding, Protein Domains, Rotavirus chemistry, Rotavirus genetics, Actins chemistry, Actins metabolism, Capsid Proteins chemistry, Capsid Proteins metabolism, Rotavirus metabolism
Abstract

The interactions between viruses and actin cytoskeleton have been widely studied. We showed that rotaviruses remodel microfilaments in intestinal cells and demonstrated that this was due to the VP4 spike protein. Microfilaments mainly occur in the apical domain of infected polarized enterocytes and favor the polarized apical exit of viral progeny. The present work aims at the identification of molecular determinants of actin-VP4 interactions. We used various deletion mutants of VP4 that were transfected into Cos-7 cells and analyzed interactions by immunofluorescence confocal microscopy. It has been established that the C-terminal part of VP4 is embedded within viral particles when rotavirus assembles. The use of specific monoclonal antibodies demonstrated that VP4 is expressed in different forms in infected cells: classically as spike on the outer layer of virus particles, but also as free soluble protein in the cytosol. The C terminus of free VP4 was identified as interacting with actin microfilaments. The VP4 actin binding domain is unable to promote microfilament remodeling by itself; the coiled-coil domain is also required in this process. This actin-binding domain was shown to dominate a previously identified peroxisomal targeting signal, located in the three last amino acids of VP4. The newly identified actin-binding domain is highly conserved in rotavirus strains from species A, B, and C, suggesting that actin binding and remodeling is a general strategy for rotavirus exit. This provides a novel mechanism of protein-protein interactions, not involving cell signaling pathways, to facilitate rotavirus exit. IMPORTANCE Rotaviruses are causal agents of acute infantile viral diarrhea. In intestinal cells, in vitro as well as in vivo , virus assembly and exit do not imply cell lysis but rely on an active process in which the cytoskeleton plays a major role. We describe here a novel molecular mechanism by which the rotavirus spike protein VP4 drives actin remodeling. This relies on the fact that VP4 occurs in different forms. Besides its structural function within the virion, a large proportion of VP4 is expressed as free protein. Here, we show that free VP4 possesses a functional actin-binding domain. This domain, in coordination with a coiled-coil domain, promotes actin cytoskeleton remodeling, thereby providing the capacity to destabilize the cell membrane and allow efficient rotavirus exit., (Copyright © 2018 American Society for Microbiology.)

Published
2018
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