Véronique Mateo
French Institute of Health and Medical Research
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Publication
Featured researches published by Véronique Mateo.
Nature | 2006
Stephanie Rigaud; Marie-Claude Fondanèche; Nathalie Lambert; Benoit Pasquier; Véronique Mateo; Pauline Soulas; Lionel Galicier; Françoise Le Deist; Frédéric Rieux-Laucat; Patrick Revy; Alain Fischer; Geneviève de Saint Basile; Sylvain Latour
The homeostasis of the immune response requires tight regulation of the proliferation and apoptosis of activated lymphocytes. In humans, defects in immune homeostasis result in lymphoproliferation disorders including autoimmunity, haemophagocytic lymphohystiocytosis and lymphomas. The X-linked lymphoproliferative syndrome (XLP) is a rare, inherited immunodeficiency that is characterized by lymphohystiocytosis, hypogammaglobulinaemia and lymphomas, and that usually develops in response to infection with Epstein–Barr virus (EBV). Mutations in the signalling lymphocyte activation molecule (SLAM)-associated protein SAP, a signalling adaptor molecule, underlie 60% of cases of familial XLP. Here, we identify mutations in the gene that encodes the X-linked inhibitor-of-apoptosis XIAP (also termed BIRC4) in patients with XLP from three families without mutations in SAP. These mutations lead to defective expression of XIAP. We show that apoptosis of lymphocytes from XIAP-deficient patients is enhanced in response to various stimuli including the T-cell antigen receptor (TCR)–CD3 complex, the death receptor CD95 (also termed Fas or Apo-1) and the TNF-associated apoptosis-inducing ligand receptor (TRAIL-R). We also found that XIAP-deficient patients, like SAP-deficient patients, have low numbers of natural killer T-lymphocytes (NKT cells), indicating that XIAP is required for the survival and/or differentiation of NKT cells. The observation that XIAP-deficiency and SAP-deficiency are both associated with a defect in NKT cells strengthens the hypothesis that NKT cells have a key role in the immune response to EBV. Furthermore, by identifying an XLP immunodeficiency that is caused by mutations in XIAP, we show that XIAP is a potent regulator of lymphocyte homeostasis in vivo.
Circulation | 2015
Amna Abderrazak; Dominique Couchie; Dler Faieeq Darweesh Mahmood; Rima Elhage; Cécile Vindis; Muriel Laffargue; Véronique Mateo; Monica Rubio Ayala; Menna El Gaafary; Tatiana Syrovets; Mohamed-Naceur Slimane; Bertrand Friguet; Tamas Fulop; Thomas Simmet; Khadija El Hadri; Mustapha Rouis
Background— This study was designed to evaluate the effect of arglabin on the NLRP3 inflammasome inhibition and atherosclerotic lesion in ApoE2Ki mice fed a high-fat Western-type diet. Methods and Results— Arglabin was purified, and its chemical identity was confirmed by mass spectrometry. It inhibited, in a concentration-dependent manner, interleukin (IL)-1&bgr; and IL-18, but not IL-6 and IL-12, production in lipopolysaccharide and cholesterol crystal–activated cultured mouse peritoneal macrophages, with a maximum effect at ≈50 nmol/L and EC50 values for both cytokines of ≈ 10 nmol/L. Lipopolysaccharide and cholesterol crystals did not induce IL-1&bgr; and IL-18 production in Nlrp3−/− macrophages. In addition, arglabin activated autophagy as evidenced by the increase in LC3-II protein. Intraperitoneal injection of arglabin (2.5 ng/g body weight twice daily for 13 weeks) into female ApoE2.Ki mice fed a high-fat diet resulted in a decreased IL-1&bgr; plasma level compared with vehicle-treated mice (5.2±1.0 versus 11.7±1.1 pg/mL). Surprisingly, arglabin also reduced plasma levels of total cholesterol and triglycerides to 41% and 42%, respectively. Moreover, arglabin oriented the proinflammatory M1 macrophages into the anti-inflammatory M2 phenotype in spleen and arterial lesions. Finally, arglabin treatment markedly reduced the median lesion areas in the sinus and whole aorta to 54% (P=0.02) and 41% (P=0.02), respectively. Conclusions— Arglabin reduces inflammation and plasma lipids, increases autophagy, and orients tissue macrophages into an anti-inflammatory phenotype in ApoE2.Ki mice fed a high-fat diet. Consequently, a marked reduction in atherosclerotic lesions was observed. Thus, arglabin may represent a promising new drug to treat inflammation and atherosclerosis.
Journal of Immunology | 2008
Anne Bristeau-Leprince; Véronique Mateo; Annick Lim; Aude Magerus-Chatinet; Eric Solary; Alain Fischer; Frédéric Rieux-Laucat; Marie-Lise Gougeon
The peripheral expansion of α/β+-CD4−CD8− double negative (DN) T cells in patients with autoimmune lymphoproliferative syndrome (ALPS) is a consistent feature of this disease, and part of the diagnostic criteria of ALPS. The origin of these cells remains undetermined. They could derive from mature T cells that have lost coreceptor expression, or represent a special minor cell lineage. To investigate relationship of DN and single positive (SP) T cells in ALPS, we used Immunoscope technology to analyze the TCRVβ repertoire diversity of sorted DN and SP T cells, and we performed CDR3 sequence analyses of matching clonotypes. We show that DN T cells express all the Vβ gene families that are used by their SP counterparts, though they dominantly use some Vβ genes. Analysis of CDR3 length distribution revealed a diverse polyclonal TCR repertoire for sorted CD4+ T cells, whereas both DN and CD8+ T cells showed a skewed TCR repertoire with oligoclonal expansions throughout most of the Vβ families. CDR3 sequencing of matching clonotypes revealed a significant sharing of CDR3 sequences from selected Vβ-Jβ transcripts between DN and CD8+ T cells. Altogether, these data strongly argue for a CD8 origin of DN T cells in ALPS.
Circulation | 2015
Amna Abderrazak; Dominique Couchie; Dler Faieeq Darweesh Mahmood; Rima El Hage; Cécile Vindis; Muriel Laffargue; Véronique Mateo; Monica Rubio Ayala; Menna El Gaafary; Tatiana Syrovets; Mohamed-Naceur Slimane; Bertrand Friguet; Tamas Fulop; Thomas Simmet; Khadija El Hadri; Mustapha Rouis
Background— This study was designed to evaluate the effect of arglabin on the NLRP3 inflammasome inhibition and atherosclerotic lesion in ApoE2Ki mice fed a high-fat Western-type diet. Methods and Results— Arglabin was purified, and its chemical identity was confirmed by mass spectrometry. It inhibited, in a concentration-dependent manner, interleukin (IL)-1&bgr; and IL-18, but not IL-6 and IL-12, production in lipopolysaccharide and cholesterol crystal–activated cultured mouse peritoneal macrophages, with a maximum effect at ≈50 nmol/L and EC50 values for both cytokines of ≈ 10 nmol/L. Lipopolysaccharide and cholesterol crystals did not induce IL-1&bgr; and IL-18 production in Nlrp3−/− macrophages. In addition, arglabin activated autophagy as evidenced by the increase in LC3-II protein. Intraperitoneal injection of arglabin (2.5 ng/g body weight twice daily for 13 weeks) into female ApoE2.Ki mice fed a high-fat diet resulted in a decreased IL-1&bgr; plasma level compared with vehicle-treated mice (5.2±1.0 versus 11.7±1.1 pg/mL). Surprisingly, arglabin also reduced plasma levels of total cholesterol and triglycerides to 41% and 42%, respectively. Moreover, arglabin oriented the proinflammatory M1 macrophages into the anti-inflammatory M2 phenotype in spleen and arterial lesions. Finally, arglabin treatment markedly reduced the median lesion areas in the sinus and whole aorta to 54% (P=0.02) and 41% (P=0.02), respectively. Conclusions— Arglabin reduces inflammation and plasma lipids, increases autophagy, and orients tissue macrophages into an anti-inflammatory phenotype in ApoE2.Ki mice fed a high-fat diet. Consequently, a marked reduction in atherosclerotic lesions was observed. Thus, arglabin may represent a promising new drug to treat inflammation and atherosclerosis.
Circulation | 2015
Amna Abderrazak; Dominique Couchie; Dler Faieeq Darweesh Mahmood; Rima Elhage; Cécile Vindis; Muriel Laffargue; Véronique Mateo; Monica Rubio Ayala; Menna El Gaafary; Tatiana Syrovets; Mohamed-Naceur Slimane; Bertrand Friguet; Tamas Fulop; Thomas Simmet; Khadija El Hadri; Mustapha Rouis
In response to the letter of Drs Takahashi and Karasawa, we thought it might be of interest to open the debate about the mechanism by which arglabin, a natural compound isolated from Artemisia glabella , inhibits cholesterol crystal–induced activation of the NLRP3 inflammasome in murine macrophages. In the March 2015 online issue of Circulation 1 we evaluated the impact of arglabin on cholesterol crystal–mediated NLRP3 activation in cultured murine macrophages and in ApoE2.Ki mice fed a high-fat diet. We showed that both Nlrp3 knockout and inhibition of NLRP3 activation by the compound arglabin significantly decreased the size of atherosclerotic lesions in ApoE2.Ki mice fed a high-fat diet. At the molecular level, arglabin inhibited the activity of the NLRP3 inflammasome and significantly reduced the subsequent production of interleukin 1β (IL-1β) and interleukin 18 in vitro …
Blood | 2002
Véronique Mateo; Eric J. Brown; Guy Biron; Manuel Rubio; Alain Fischer; Françoise Le Deist; Marika Sarfati
Blood | 2003
Marika Sarfati; Véronique Mateo; Sylvie Baudet; Manuel Rubio; Christine Fernandez; Frederic Davi; Jacques L. Binet; Jozo Delic; Hélène Merle-Béral
The New England Journal of Medicine | 2006
Frédéric Rieux-Laucat; Claire Hivroz; Annick Lim; Véronique Mateo; Isabelle Pellier; Françoise Selz; Alain Fischer; Françoise Le Deist
Journal of Immunology | 1997
Sylvie Lesage; Ann-Muriel Steff; Fabianne Philippoussis; M Pagé; S Trop; Véronique Mateo; Patrice Hugo
Blood | 2003
Fabianne Philippoussis; Chantal Arguin; Véronique Mateo; Ann-Muriel Steff; Patrice Hugo