19 results on '"Groyer, Emilie"'
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2. Aspects immunologiques de l’athérome
- Author
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Groyer, Émilie, Caligiuri, Giuseppina, Laschet-Khallou, Jamila, and Nicoletti, Antonino
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- 2006
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3. A CD31-derived peptide prevents angiotensin II-induced atherosclerosis progression and aneurysm formation
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Fornasa, Giulia, Clement, Marc, Groyer, Emilie, Gaston, Anh-Thu, Khallou-Laschet, Jamila, Morvan, Marion, Guedj, Kevin, Kaveri, Srini V., Tedgui, Alain, Michel, Jean-Baptiste, Nicoletti, Antonino, and Caligiuri, Giuseppina
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- 2012
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4. TCR stimulation drives cleavage and shedding of the ITIM receptor CD31
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Fornasa, Giulia, Groyer, Emilie, Clement, Marc, Dimitrov, Jordan, Compain, Caroline, Gaston, Anh-Thu, Varthaman, Aditi, Khallou-Laschet, Jamila, Newman, Debra, Graff-Dubois, Stéphanie, Nicoletti, Antonino, Caligiuri, Giuseppina, Hémostase, bio-ingénierie et remodelage cardiovasculaires (LBPC), Université Paris Diderot - Paris 7 (UPD7)-Université Paris 13 (UP13)-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Galilée, Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Paris Descartes - Paris 5 (UPD5)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Blood Research Institute, BloodCenter of Wisconsin, Immunité et Infection, Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR113-Université Pierre et Marie Curie - Paris 6 (UPMC), This work was supported in part by grants from the 'Fondation de France' (Engt 2006-005656 and 2008- 002724), the 'Fondation pour la Recherche Médicale' (DCV20070409268) and the 'Agence Nationale de la Recherche' (project 'RELATE' and project 'BROSCI'). G.F. is the recipient of a training grant from the 'Ministère affaires étrangères' (Egide N°636511F) and of the 'Groupe de Reflexion sur la Recherche Cardio-vasculaire et la Féderation Française de Cardiologie'. E.G. was the recipient of a research grant from the 'Fondation pour la Recherche Médicale' (FDT20071211595)., ANR: project 'RELATE and 'BROSCI',project 'RELATE and 'BROSCI', Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR113-Institut National de la Santé et de la Recherche Médicale (INSERM), Hémostase, bio-ingénierie et remodelage cardiovasculaires ( LBPC ), Université Paris 13 ( UP13 ) -Université Paris Diderot - Paris 7 ( UPD7 ) -Université Sorbonne Paris Cité ( USPC ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Institut Galilée, Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -IFR113-Institut National de la Santé et de la Recherche Médicale ( INSERM ), ANR : project 'RELATE and 'BROSCI',project 'RELATE and 'BROSCI', Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut Galilée-Université Sorbonne Paris Cité (USPC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), and ANR-07-PHYS-0021,RELATE,Regulation des lymphocytes dans les manifestations atherothrombotiques(2007)
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MESH : Molecular Sequence Data ,MESH: Immunoglobulins ,MESH : Cell Membrane ,MESH: Mice, Inbred BALB C ,MESH : Mice, Inbred C57BL ,MESH: Amino Acid Sequence ,MESH: T-Lymphocyte Subsets ,MESH: Mice, Knockout ,MESH : Receptors, Antigen, T-Cell ,MESH : Extracellular Space ,MESH : Immunoglobulins ,MESH: Protein Structure, Tertiary ,MESH: Mice, Inbred C57BL ,MESH : Mice ,MESH : Cells, Cultured ,MESH: Jurkat Cells ,[ SDV.IMM ] Life Sciences [q-bio]/Immunology ,MESH: Animals ,MESH: Peptide Fragments ,MESH: Lymphocyte Activation ,MESH: Mice ,MESH : Mice, Inbred BALB C ,MESH : Jurkat Cells ,MESH : Lymphocyte Activation ,MESH: Molecular Sequence Data ,MESH: Humans ,MESH : Amino Acid Sequence ,MESH : Peptide Fragments ,MESH : Humans ,MESH: Receptors, Antigen, T-Cell ,MESH: Antigens, CD31 ,MESH : T-Lymphocyte Subsets ,MESH: Extracellular Space ,MESH : Antigens, CD31 ,cardiovascular system ,MESH : Mice, Knockout ,[SDV.IMM]Life Sciences [q-bio]/Immunology ,MESH : Animals ,MESH : Protein Structure, Tertiary ,MESH: Cell Membrane ,MESH: Cells, Cultured - Abstract
International audience; CD31 is a transmembrane molecule endowed with T cell regulatory functions owing to the presence of 2 immunotyrosine-based inhibitory motifs. For reasons not understood, CD31 is lost by a portion of circulating T lymphocytes, which appear prone to uncontrolled activation. In this study, we show that extracellular T cell CD31 comprising Ig-like domains 1 to 5 is cleaved and shed from the surface of human T cells upon activation via their TCR. The shed CD31 can be specifically detected as a soluble, truncated protein in human plasma. CD31 shedding results in the loss of its inhibitory function because the necessary cis-homo-oligomerization of the molecule, triggered by the trans-homophilic engagement of the distal Ig-like domain 1, cannot be established by CD31(shed) cells. However, we show that a juxta-membrane extracellular sequence, comprising part of the domain 6, remains expressed at the surface of CD31(shed) T cells. We also show that the immunosuppressive CD31 peptide aa 551-574 is highly homophilic and possibly acts by homo-oligomerizing with the truncated CD31 remaining after its cleavage and shedding. This peptide is able to sustain phosphorylation of the CD31 ITIM(686) and of SHP2 and to inhibit TCR-induced T cell activation. Finally, systemic administration of the peptide in BALB/c mice efficiently suppresses Ag-induced T cell-mediated immune responses in vivo. We conclude that the loss of T cell regulation caused by CD31 shedding driven by TCR stimulation can be rescued by molecular tools able to engage the truncated juxta-membrane extracellular molecule that remains exposed at the surface of CD31(shed) cells.
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- 2010
5. Antiangiogenic Treatment Prevents Adventitial Constrictive Remodeling in Graft Arteriosclerosis.
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Thaunat, Olivier, Louedec, Liliane, Graff-Dubois, Stéphanie, Dai, Jiangping, Groyer, Emilie, Yacoub-Youssef, Houda, Mandet, Chantal, Bruneval, Patrick, Kaveri, Srini, Caligiuri, Giuseppina, Germain, Stéphane, Michel, Jean-Baptiste, and Nicoletti, Antonino
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- 2008
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6. TCR stimulation drives cleavage and shedding of the ITIM receptor CD31.
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Fornasa G, Groyer E, Clement M, Dimitrov J, Compain C, Gaston AT, Varthaman A, Khallou-Laschet J, Newman DK, Graff-Dubois S, Nicoletti A, and Caligiuri G
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- Amino Acid Sequence, Animals, Cell Membrane immunology, Cell Membrane metabolism, Cells, Cultured, Extracellular Space immunology, Extracellular Space metabolism, Humans, Immunoglobulins metabolism, Jurkat Cells, Lymphocyte Activation immunology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Molecular Sequence Data, Peptide Fragments chemical synthesis, Peptide Fragments genetics, Platelet Endothelial Cell Adhesion Molecule-1 biosynthesis, Platelet Endothelial Cell Adhesion Molecule-1 genetics, Protein Structure, Tertiary, Peptide Fragments metabolism, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Receptors, Antigen, T-Cell metabolism, Receptors, Antigen, T-Cell physiology, T-Lymphocyte Subsets immunology, T-Lymphocyte Subsets metabolism
- Abstract
CD31 is a transmembrane molecule endowed with T cell regulatory functions owing to the presence of 2 immunotyrosine-based inhibitory motifs. For reasons not understood, CD31 is lost by a portion of circulating T lymphocytes, which appear prone to uncontrolled activation. In this study, we show that extracellular T cell CD31 comprising Ig-like domains 1 to 5 is cleaved and shed from the surface of human T cells upon activation via their TCR. The shed CD31 can be specifically detected as a soluble, truncated protein in human plasma. CD31 shedding results in the loss of its inhibitory function because the necessary cis-homo-oligomerization of the molecule, triggered by the trans-homophilic engagement of the distal Ig-like domain 1, cannot be established by CD31(shed) cells. However, we show that a juxta-membrane extracellular sequence, comprising part of the domain 6, remains expressed at the surface of CD31(shed) T cells. We also show that the immunosuppressive CD31 peptide aa 551-574 is highly homophilic and possibly acts by homo-oligomerizing with the truncated CD31 remaining after its cleavage and shedding. This peptide is able to sustain phosphorylation of the CD31 ITIM(686) and of SHP2 and to inhibit TCR-induced T cell activation. Finally, systemic administration of the peptide in BALB/c mice efficiently suppresses Ag-induced T cell-mediated immune responses in vivo. We conclude that the loss of T cell regulation caused by CD31 shedding driven by TCR stimulation can be rescued by molecular tools able to engage the truncated juxta-membrane extracellular molecule that remains exposed at the surface of CD31(shed) cells.
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- 2010
- Full Text
- View/download PDF
7. Direct and indirect effects of alloantibodies link neointimal and medial remodeling in graft arteriosclerosis.
- Author
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Thaunat O, Louedec L, Dai J, Bellier F, Groyer E, Delignat S, Gaston AT, Caligiuri G, Joly E, Plissonnier D, Michel JB, and Nicoletti A
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- Animals, Aorta immunology, Aorta physiopathology, Arteriosclerosis immunology, Cell Proliferation drug effects, Cell Survival, Cells, Cultured, Chronic Disease, Culture Media, Conditioned pharmacology, Graft Occlusion, Vascular immunology, Graft Rejection immunology, Graft Rejection pathology, Growth Substances genetics, Isoantibodies biosynthesis, Isoantibodies pharmacology, Kinetics, Major Histocompatibility Complex immunology, Male, Myocytes, Smooth Muscle pathology, Rats, Rats, Inbred BN, Rats, Inbred Lew, Tissue Donors, Transcription, Genetic, Transplantation Chimera, Tunica Intima immunology, Tunica Media immunology, Up-Regulation drug effects, Arteriosclerosis physiopathology, Graft Occlusion, Vascular physiopathology, Graft Rejection physiopathology, Isoantibodies immunology, Tunica Intima physiopathology, Tunica Media physiopathology
- Abstract
Objective: Chronic vascular rejection, the main cause of allograft failure, is characterized by the destruction of smooth muscle cells (SMCs) in the media concomitantly with the proliferation of SMCs in the adjacent neointima. We hypothesized that alloantibodies might be responsible for these 2 opposite but coordinated events., Methods and Results: We used the rat aortic interposition model of chronic vascular rejection. During the rejection process, a neointima composed of proliferating SMCs from the recipient developed, whereas the SMCs in the media, all of donor origin, underwent apoptosis. Alloantibody deposition was detected only in the media. Using in vitro cultures experiments, we observed that alloantibody binding to donor SMCs exerts (1) a rapid upregulation of the transcription of growth factors genes, followed by (2) the induction of apoptosis after 24 hours. The transient production of growth factors by donor SMCs in response to the binding of alloantibodies induced the proliferation of recipient SMCs in culture supernatant transfer experiments. Additional data suggest that among the repertoire of alloantibodies, those directed against major histocompatibility complex I might carry the remodeling effect., Conclusions: Our data suggest that during chronic vascular rejection, alloantibody binding to donor medial SMCs is a crucial event that links neointimal and medial remodeling.
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- 2006
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8. [Immunological aspects of atherosclerosis].
- Author
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Groyer E, Caligiuri G, Laschet-Khallou J, and Nicoletti A
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- Apolipoproteins E metabolism, B-Lymphocytes immunology, Coronary Artery Disease metabolism, Humans, Lipoproteins, LDL metabolism, Antibodies, Antiphospholipid immunology, CD4 Antigens immunology, Coronary Artery Disease immunology, Cytokines immunology, Interferon-gamma immunology, Killer Cells, Natural immunology, Th1 Cells immunology, Th2 Cells immunology
- Abstract
The pathogenesis of atherosclerosis remains incompletely understood. Accumulation of oxidized lipoproteins (oxLDL) within the vascular wall drives a related immune response very early during the disease course. Such an immune response is self-amplified and eventually escapes from physiologic control mechanisms. Certain lymphocytes may become pathogenic. B cells play a protective role by producing antibodies able to neutralize oxLDL. Elucidation of the immune control mechanisms in atherosclerosis will open the way to new therapeutic perspectives., ((c) 2006, Masson, Paris.)
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- 2006
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9. Reduced immunoregulatory CD31+ T cells in patients with atherosclerotic abdominal aortic aneurysm.
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Caligiuri G, Rossignol P, Julia P, Groyer E, Mouradian D, Urbain D, Misra N, Ollivier V, Sapoval M, Boutouyrie P, Kaveri SV, Nicoletti A, and Lafont A
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- Aged, Aged, 80 and over, Aortic Aneurysm, Abdominal pathology, Atherosclerosis pathology, CD4-CD8 Ratio, CD4-Positive T-Lymphocytes metabolism, CD8-Positive T-Lymphocytes immunology, Female, Humans, Lymphocyte Activation immunology, Macrophages immunology, Male, Middle Aged, Aortic Aneurysm, Abdominal immunology, Atherosclerosis immunology, CD4-Positive T-Lymphocytes immunology, Platelet Endothelial Cell Adhesion Molecule-1 metabolism
- Abstract
Background: Cell-mediated immunity is considered to contribute to the pathogenesis of abdominal aortic aneurysms (AAA). In particular, infiltrating macrophages and CD8+ T lymphocytes participate in the destruction of the aortic wall extracellular matrix and smooth muscle cells. We surmise that these pathological events are controlled by circulating regulatory lymphocytes., Methods and Results: Circulating CD4+/CD31+ cells were reduced in AAA patients (n=80, 8.9+/-0.6%) as compared with controls (n=69, 13.7+/-0.8%; P<0.001) and inversely proportional to AAA size. Exclusion of the aneurysm by an endoprothesis did not affect CD31+ T cell values. Reduction of blood CD4+/CD31+ cells was not attributable to their enrichment in AAA tissue. In contrast, CD8+/CD31+ cells were slightly reduced in the blood while increased in the aneurysmal tissue (29.2+/-0.5 versus 20.2+/-4.7% in blood, n=6; P<0.05). Remarkably, high percentages of CD4+/CD31+ cells were able to regulate proliferation and cytokine production of CD8+ lymphocytes, as well as CD8+ cell-mediated cytotoxicity of aortic smooth muscle cells (P<0.01). Finally, CD4+/CD31+ cells reduced the production and activity of metalloproteinase-9 by lipopolysaccharide-stimulated macrophages., Conclusions: Circulating CD4+/CD31+ T cells regulate macrophage and CD8+ T cell activation and effector function in the arterial wall. Their reduction might promote the development of AAA.
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- 2006
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10. The proatherogenic role of T cells requires cell division and is dependent on the stage of the disease.
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Khallou-Laschet J, Caligiuri G, Groyer E, Tupin E, Gaston AT, Poirier B, Kronenberg M, Cohen JL, Klatzmann D, Kaveri SV, and Nicoletti A
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- Animals, Antiviral Agents, Aorta immunology, Aorta pathology, Apolipoproteins E genetics, Cell Division drug effects, Cell Division immunology, Disease Progression, Female, Ganciclovir, Gene Expression drug effects, Herpesvirus 1, Human genetics, Killer Cells, Natural pathology, Killer Cells, Natural physiology, Mice, Mice, Inbred Strains, Mice, Transgenic, Thymidine Kinase genetics, Transgenes physiology, Atherosclerosis immunology, Atherosclerosis pathology, T-Lymphocytes pathology, T-Lymphocytes physiology
- Abstract
Objective: The mechanism by which T cells exert a proatherogenic potential is unclear. In order to determine whether this potential requires their replication, we crossed atherosclerosis-prone apolipoprotein E knockout mice (ApoE degrees) with transgenic mice in which exclusive and conditional ablation of dividing T cells relies on their specific expression of the herpes simplex type 1 thymidine kinase (TK) suicide gene., Methods and Results: We first showed that conalbumin-immunized ApoE degrees TK mice mounted a significant immune response to the antigen that was fully and specifically blocked by an in vivo ganciclovir (GCV) treatment. Next, ApoE degrees TK mice and ApoE degrees mice were treated or not with GCV either during the first 4 weeks (GCV 1 to 4w), the last 4 weeks (GCV 5 to 8w), or during 8 weeks (GCV 1 to 8w). Strikingly, ApoE degrees TK mice displayed a dramatic decrease in lesion development in the GCV 1 to 8w and GCV 5 to 8w groups, whereas the GCV had no effect when administered during the first 4 weeks. In protected mice, the inflammatory parameters in lesions, the percentage of CD69+ CD3+ splenocytes, and the circulating natural killer T cells were reduced., Conclusions: The present study, therefore, shows that the proatherogenic potential of T cells is crucial in the progression of fatty streaks to mature plaques and requires cell division.
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- 2006
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11. Reduced immunoregulatory CD31+ T cells in the blood of atherosclerotic mice with plaque thrombosis.
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Caligiuri G, Groyer E, Khallou-Laschet J, Al Haj Zen A, Sainz J, Urbain D, Gaston AT, Lemitre M, Nicoletti A, and Lafont A
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- Animals, Apolipoproteins E genetics, Atherosclerosis pathology, Biomarkers, Female, Immunohistochemistry, Lymphocyte Count, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Platelet Endothelial Cell Adhesion Molecule-1 metabolism, Rupture, T-Lymphocytes cytology, T-Lymphocytes metabolism, Thrombosis pathology, Atherosclerosis immunology, Lymphocyte Activation immunology, T-Lymphocytes immunology, Thrombosis immunology
- Abstract
Objective: Lymphocyte activation is thought to play a major role in the pathogenesis of atherosclerotic complications such as plaque thrombosis. Circulating CD31+ T cells have been shown to regulate human T cell activation. Aim of this study was to evaluate whether the proportion of circulating immunoregulatory CD31+ T cells is correlated to the occurrence of plaque thrombosis in aged apolipoprotein (apo) E knockout (KO) mice., Methods and Results: CD31+ T cell depletion of spleen T cells enhanced proliferation (P<0.05) and interferon-gamma production (P<0.01) while reducing interleukin (IL)-4 (P<0.001) and IL-10 (P=0.001) secretion in response to minimally modified low-density lipoprotein. CD31+ T cells were counted in 65 apoE KO mice (46-week-old) by flow cytometry. Organizing thrombi could be documented in 28 of 195 (14%) lesions and in at least one of the aorta root lesions in 23 of 65 mice (35%). CD31+ T cell count was significantly reduced in mice showing plaque thrombosis (72.3+/-1.5% versus 84.1+/-1.2%; P<0.0001), but such reduction did not follow induced plaque rupture or experimentally controlled thrombosis., Conclusions: Reduced CD31+ T cells in circulating blood is a hallmark of atherosclerotic plaque thrombosis. Our data suggest that CD31+ T cells may play an important regulatory role in the development of plaque thrombosis.
- Published
- 2005
- Full Text
- View/download PDF
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