Publications
2007
Woods Anne, Monneaux Fanny, Soulas-Sprauel Pauline, Muller Sylviane, Martin Thierry, Korganow Anne-Sophie, Pasquali Jean-Louis
Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance Article de journal
Dans: Journal of Virology, vol. 81, no. 22, p. 12525–12534, 2007, ISSN: 0022-538X.
Résumé | Liens | BibTeX | Étiquettes: Animals, Antibody Formation, Autoantibodies, Autoantigens, Autoimmunity, B-Lymphocytes, Humans, I2CT, Immune Tolerance, Immunoglobulin M, Inbred Strains, Influenza A virus, Interferon Type I, Lymphocyte Activation, Mice, Monneaux, Rheumatoid Factor, Team-Dumortier, transgenic
@article{woods_influenza_2007,
title = {Influenza virus-induced type I interferon leads to polyclonal B-cell activation but does not break down B-cell tolerance},
author = {Anne Woods and Fanny Monneaux and Pauline Soulas-Sprauel and Sylviane Muller and Thierry Martin and Anne-Sophie Korganow and Jean-Louis Pasquali},
doi = {10.1128/JVI.00839-07},
issn = {0022-538X},
year = {2007},
date = {2007-01-01},
journal = {Journal of Virology},
volume = {81},
number = {22},
pages = {12525--12534},
abstract = {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.},
keywords = {Animals, Antibody Formation, Autoantibodies, Autoantigens, Autoimmunity, B-Lymphocytes, Humans, I2CT, Immune Tolerance, Immunoglobulin M, Inbred Strains, Influenza A virus, Interferon Type I, Lymphocyte Activation, Mice, Monneaux, Rheumatoid Factor, Team-Dumortier, transgenic},
pubstate = {published},
tppubtype = {article}
}
2006
Gottar Marie, Gobert Vanessa, Matskevich Alexey A, Reichhart Jean-Marc, Wang Chengshu, Butt Tariq M, Belvin Marcia, Hoffmann Jules A, Ferrandon Dominique
Dual detection of fungal infections in Drosophila via recognition of glucans and sensing of virulence factors Article de journal
Dans: Cell, vol. 127, no. 7, p. 1425–1437, 2006, ISSN: 0092-8674.
Résumé | Liens | BibTeX | Étiquettes: Animals, Antibody Formation, Beauveria, Candida albicans, Carrier Proteins, Cellular, ferrandon, Glucans, hoffmann, Immunity, Immunological, M3i, Metarhizium, Models, Polysaccharides, reichhart, Serine Endopeptidases, Signal Transduction, Virulence Factors
@article{gottar_dual_2006,
title = {Dual detection of fungal infections in Drosophila via recognition of glucans and sensing of virulence factors},
author = {Marie Gottar and Vanessa Gobert and Alexey A Matskevich and Jean-Marc Reichhart and Chengshu Wang and Tariq M Butt and Marcia Belvin and Jules A Hoffmann and Dominique Ferrandon},
doi = {10.1016/j.cell.2006.10.046},
issn = {0092-8674},
year = {2006},
date = {2006-12-01},
journal = {Cell},
volume = {127},
number = {7},
pages = {1425--1437},
abstract = {The Drosophila immune system discriminates between various types of infections and activates appropriate signal transduction pathways to combat the invading microorganisms. The Toll pathway is required for the host response against fungal and most Gram-positive bacterial infections. The sensing of Gram-positive bacteria is mediated by the pattern recognition receptors PGRP-SA and GNBP1 that cooperate to detect the presence of infections in the host. Here, we report that GNBP3 is a pattern recognition receptor that is required for the detection of fungal cell wall components. Strikingly, we find that there is a second, parallel pathway acting jointly with GNBP3. The Drosophila Persephone protease activates the Toll pathway when proteolytically matured by the secreted fungal virulence factor PR1. Thus, the detection of fungal infections in Drosophila relies both on the recognition of invariant microbial patterns and on monitoring the effects of virulence factors on the host.},
keywords = {Animals, Antibody Formation, Beauveria, Candida albicans, Carrier Proteins, Cellular, ferrandon, Glucans, hoffmann, Immunity, Immunological, M3i, Metarhizium, Models, Polysaccharides, reichhart, Serine Endopeptidases, Signal Transduction, Virulence Factors},
pubstate = {published},
tppubtype = {article}
}
2005
Hayer Silvia, Tohidast-Akrad Makiyeh, Haralambous Silva, Jahn-Schmid Beatrice, Skriner Karl, Trembleau Sylvie, Dumortier Hélène, Pinol-Roma Serafin, Redlich Kurt, Schett Georg, Muller Sylviane, Kollias George, Smolen Josef, Steiner Günter
Dans: Journal of Immunology (Baltimore, Md.: 1950), vol. 175, no. 12, p. 8327–8336, 2005, ISSN: 0022-1767.
Résumé | Liens | BibTeX | Étiquettes: Animals, Antibody Formation, arthritis, Autoantibodies, Autoantigens, Dumortier, Gene Expression Regulation, Heterogeneous-Nuclear Ribonucleoprotein Group A-B, Humans, I2CT, Joints, Mice, rheumatoid, Team-Dumortier, Tissue Distribution, transgenic, Tumor Necrosis Factor-alpha
@article{hayer_aberrant_2005,
title = {Aberrant expression of the autoantigen heterogeneous nuclear ribonucleoprotein-A2 (RA33) and spontaneous formation of rheumatoid arthritis-associated anti-RA33 autoantibodies in TNF-alpha transgenic mice},
author = {Silvia Hayer and Makiyeh Tohidast-Akrad and Silva Haralambous and Beatrice Jahn-Schmid and Karl Skriner and Sylvie Trembleau and Hélène Dumortier and Serafin Pinol-Roma and Kurt Redlich and Georg Schett and Sylviane Muller and George Kollias and Josef Smolen and Günter Steiner},
doi = {10.4049/jimmunol.175.12.8327},
issn = {0022-1767},
year = {2005},
date = {2005-12-01},
journal = {Journal of Immunology (Baltimore, Md.: 1950)},
volume = {175},
number = {12},
pages = {8327--8336},
abstract = {Human TNF-alpha transgenic (hTNFtg) mice develop erosive arthritis closely resembling rheumatoid arthritis (RA). To investigate mechanisms leading to pathological autoimmune reactions in RA, we examined hTNFtg animals for the presence of RA-associated autoantibodies including Abs to citrullinated epitopes (anti-cyclic citrullinated peptide), heterogeneous nuclear ribonucleoprotein (hnRNP)-A2 (anti-RA33), and heat shock proteins (hsp) (anti-hsp). Although IgM anti-hsp Abs were detected in 40% of hTNFtg and control mice, IgG anti-hsp Abs were rarely seen, and anti-cyclic citrullinated peptide Abs were not seen at all. In contrast, textgreater50% of hTNFtg mice showed IgG anti-RA33 autoantibodies, which became detectable shortly after the onset of arthritis. These Abs were predominantly directed to a short epitope, which was identical with an epitope previously described in MRL/lpr mice. Incidence of anti-RA33 was significantly decreased in mice treated with the osteoclast inhibitor osteoprotegerin and also in c-fos-deficient mice lacking osteoclasts. Pronounced expression of hnRNP-A2 and a smaller splice variant was seen in joints of hTNFtg mice, whereas expression was low in control animals. Although the closely related hnRNP-A1 was also overexpressed, autoantibodies to this protein were infrequently detected. Because expression of hnRNP-A2 in thymus, spleen, brain, and lung was similar in hTNFtg and control mice, aberrant expression appeared to be restricted to the inflamed joint. Finally, immunization of hTNFtg mice with recombinant hnRNP-A2 or a peptide harboring the major B cell epitope aggravated arthritis. These findings suggest that overproduction of TNF-alpha leads to aberrant expression of hnRNP-A2 in the rheumatoid joint and subsequently to autoimmune reactions, which may enhance the inflammatory and destructive process.},
keywords = {Animals, Antibody Formation, arthritis, Autoantibodies, Autoantigens, Dumortier, Gene Expression Regulation, Heterogeneous-Nuclear Ribonucleoprotein Group A-B, Humans, I2CT, Joints, Mice, rheumatoid, Team-Dumortier, Tissue Distribution, transgenic, Tumor Necrosis Factor-alpha},
pubstate = {published},
tppubtype = {article}
}
2003
Sabatier Laurence, Jouanguy Emmanuelle, Dostert Catherine, Zachary Daniel, Dimarcq Jean-Luc, Bulet Philippe, Imler Jean-Luc
Pherokine-2 and -3 Article de journal
Dans: European journal of biochemistry / FEBS, vol. 270, no. 16, p. 3398–3407, 2003, ISSN: 0014-2956.
Résumé | BibTeX | Étiquettes: Animals, Antibody Formation, Base Sequence, Hemolymph, imler, M3i, Mass, Matrix-Assisted Laser Desorption-Ionization, Spectrometry
@article{sabatier_pherokine-2_2003,
title = {Pherokine-2 and -3},
author = {Laurence Sabatier and Emmanuelle Jouanguy and Catherine Dostert and Daniel Zachary and Jean-Luc Dimarcq and Philippe Bulet and Jean-Luc Imler},
issn = {0014-2956},
year = {2003},
date = {2003-01-01},
journal = {European journal of biochemistry / FEBS},
volume = {270},
number = {16},
pages = {3398--3407},
abstract = {Drosophila is a powerful model system to study the regulatory and effector mechanisms of innate immunity. To identify molecules induced in the course of viral infection in this insect, we have developed a model based on intrathoracic injection of the picorna-like Drosophila C virus (DCV). We have used MALDI-TOF mass spectrometry to compare the hemolymph of DCV infected flies and control flies. By contrast with the strong humoral response triggered by injection of bacteria or fungal spores, we have identified only one molecule induced in the hemolymph of virus infected flies. This molecule, pherokine-2 (Phk-2), is related to OS-D/A10 (Phk-1), which was previously characterized as a putative odor/pheromone binding protein specifically expressed in antennae. The virus-induced molecule is also similar to the product of the gene CG9358 (Phk-3), which is induced by septic injury. Both Phk-2 and Phk-3 are strongly expressed during metamorphosis, suggesting that they may participate in tissue-remodeling.},
keywords = {Animals, Antibody Formation, Base Sequence, Hemolymph, imler, M3i, Mass, Matrix-Assisted Laser Desorption-Ionization, Spectrometry},
pubstate = {published},
tppubtype = {article}
}
1991
Bulet Philippe, Cociancich S, Dimarcq Jean-Luc, Lambert J, Reichhart Jean-Marc, Hoffmann Danièle, Hetru Charles, Hoffmann Jules A
Insect immunity. Isolation from a coleopteran insect of a novel inducible antibacterial peptide and of new members of the insect defensin family Article de journal
Dans: J. Biol. Chem., vol. 266, no. 36, p. 24520–24525, 1991, ISSN: 0021-9258.
Résumé | BibTeX | Étiquettes: Animals, Antibody Formation, Beetles, Blood Bactericidal Activity, Blood Proteins, Chromatography, Defensins, Hemolymph, High Pressure Liquid, hoffmann, Insect Hormones, Insect Proteins, M3i, reichhart
@article{bulet_insect_1991,
title = {Insect immunity. Isolation from a coleopteran insect of a novel inducible antibacterial peptide and of new members of the insect defensin family},
author = {Philippe Bulet and S Cociancich and Jean-Luc Dimarcq and J Lambert and Jean-Marc Reichhart and Danièle Hoffmann and Charles Hetru and Jules A Hoffmann},
issn = {0021-9258},
year = {1991},
date = {1991-12-01},
journal = {J. Biol. Chem.},
volume = {266},
number = {36},
pages = {24520--24525},
abstract = {Injection of heat-killed bacteria into larvae of the large tenebrionid beetle Zophobas atratus (Insecta, Endopterygota, Coleoptera) results in the appearance in the hemolymph of a potent antibacterial activity as evidenced by a plate growth inhibition assay. We have isolated three peptides (A-C) from this immune hemolymph which probably account for most of this activity. Their primary structures were established by a combination of peptide sequencing and molecular mass determination by mass spectrometry. Peptide A, which is bactericidal against Gram-negative cells, is a 74-residue glycine-rich molecule with no sequence homology to known peptides. We propose the name coleoptericin for this novel inducible antibacterial peptide. Peptides B and C are isoforms of a 43-residue peptide which contains 6 cysteines and shows significant sequence homology to insect defensins, initially reported from dipteran insects. This peptide is active against Gram-positive bacteria. The results are discussed in connection with recent studies on inducible antibacterial peptides present in the three other major orders of the endopterygote clade of insects: the Lepidoptera, Diptera, and Hymenoptera.},
keywords = {Animals, Antibody Formation, Beetles, Blood Bactericidal Activity, Blood Proteins, Chromatography, Defensins, Hemolymph, High Pressure Liquid, hoffmann, Insect Hormones, Insect Proteins, M3i, reichhart},
pubstate = {published},
tppubtype = {article}
}