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1. Full Text Complement system part II: Role in immunity
by Merle, Nicolas S and Noe, Remi and Halbwachs-Mecarelli, Lise and Fremeaux-Bacchi, Veronique and Roumenina, Lubka T
Frontiers in Immunology, ISSN 1664-3224, 2015, Volume 6, Issue MAY, p. 257
The complement system has been considered for a long time as a simple lytic cascade, aimed to kill bacteria infecting the host organism. Nowadays, this vision... 
Complement and innate immunity | Crosstalk TLR-complement | Anaphylatoxins | Pathogen strategies for immune evasion | Adaptive immunity | Complement system | Complement-related diseases | Complement in cancer | HEMOLYTIC-UREMIC SYNDROME | MANNOSE-BINDING LECTIN | complement system | complement and innate immunity | complement-related diseases | PAROXYSMAL-NOCTURNAL HEMOGLOBINURIA | IMMUNOLOGY | crosstalk TLR-complement | adaptive immunity | FACTOR-H-AUTOANTIBODIES | ANTIGEN-SPECIFIC T | DENSE DEPOSIT DISEASE | T-CELL RESPONSES | pathogen strategies for immune evasion | STAPHYLOCOCCUS-AUREUS PROTEIN | anaphylatoxins | complement in cancer | DECAY-ACCELERATING FACTOR | C3A ANAPHYLATOXIN RECEPTOR | Life Sciences | Immunology | Adaptive Immunity | atypical hemolytic uremic syndrome (aHUS) | innate immunity | Complement C3 | Phagocytosis
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2. Full Text Inhibition of the mTORC Pathway in the Antiphospholipid Syndrome
by Canaud, Guillaume and Bienaimé, Frank and Tabarin, Fanny and Bataillon, Guillaume and Seilhean, Danielle and Noël, Laure-Hélène and Dragon-Durey, Marie-Agnès and Snanoudj, Renaud and Friedlander, Gérard and Halbwachs-Mecarelli, Lise and Legendre, Christophe and Terzi, Fabiola
The New England Journal of Medicine, ISSN 0028-4793, 07/2014, Volume 371, Issue 4, pp. 303 - 312
This study shows that the mTORC pathway is central to the antiphospholipid syndrome. Among patients with kidney transplants and antiphospholipid syndrome, 70%... 
RAPAMYCIN | BETA-GLYCOPROTEIN-I | MEDICINE, GENERAL & INTERNAL | SYSTEMIC-LUPUS-ERYTHEMATOSUS | ANGIOPLASTY | ANTIBODY-MEDIATED REJECTION | POLYCYSTIC KIDNEY-DISEASE | SMOOTH-MUSCLE-CELLS | ANTI-BETA-GLYCOPROTEIN-I ANTIBODIES | SYNDROME NEPHROPATHY | VASCULOPATHY | Endothelium, Vascular - cytology | Cell Proliferation | Kidney - blood supply | Kidney - pathology | TOR Serine-Threonine Kinases - metabolism | Humans | Immunoglobulin G | Immunosuppressive Agents - therapeutic use | Middle Aged | Male | Antiphospholipid Syndrome - complications | TOR Serine-Threonine Kinases - antagonists & inhibitors | Autopsy | Adult | Female | Antiphospholipid Syndrome - metabolism | Immunosuppressive Agents - pharmacology | Kidney Diseases - metabolism | Sirolimus - therapeutic use | Antiphospholipid Syndrome - drug therapy | Kidney Transplantation | Sirolimus - pharmacology | Antibodies, Antiphospholipid - metabolism | Analysis of Variance | Endothelium, Vascular - metabolism | Endothelium, Vascular - pathology | Kidney Diseases - etiology | Metabolic Networks and Pathways - drug effects | Care and treatment | Rapamycin | Health aspects | Antiphospholipid syndrome | TOR protein | Cell proliferation | Lupus | Heart attacks | Kidneys | Transplants & implants | Sirolimus | AKT protein | Antiphospholipid antibodies | Kinases | Thrombosis | Endothelial cells | Endothelium | 1-Phosphatidylinositol 3-kinase | Vascular diseases | Nephropathy | Biopsy | Autoimmune diseases | Kidney transplantation
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3. Full Text Human neutrophil integrin α9β1: up-regulation by cell activation and synergy with β2 integrins during adhesion to endothelium under flow
by Agnès Mambole and Sylvain Bigot and Dominique Baruch and Philippe Lesavre and Lise Halbwachs-Mecarelli
Journal of Leukocyte Biology, ISSN 0741-5400, 08/2010, Volume 88, Issue 2, pp. 321 - 327
α9β1 is the main β1 integrin of human activated neutrophils; and α9β1/VCAM‐1 interactions participate to neutrophilrolling on endothelial cells. Neutrophil β1... 
rolling | VCAM‐1 | endothelial cells | Rolling | VCAM-1 | Endothelial cells
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4. Full Text Neutrophils: Molecules, Functions and Pathophysiological Aspects
by Witko-Sarsat, Véronique and Rieu, Philippe and Descamps-Latscha, Béatrice and Lesavre, Philippe and Halbwachs-Mecarelli, Lise
Laboratory Investigation, ISSN 0023-6837, 05/2000, Volume 80, Issue 5, pp. 617 - 653
MEDICINE, RESEARCH & EXPERIMENTAL | TUMOR-NECROSIS-FACTOR | SELECTIN GLYCOPROTEIN LIGAND-1 | INTERCELLULAR-ADHESION MOLECULE-1 | FC-GAMMA RECEPTORS | CHRONIC GRANULOMATOUS-DISEASE | PERMEABILITY-INCREASING PROTEIN | NITRIC-OXIDE SYNTHASE | ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES | PATHOLOGY | HUMAN POLYMORPHONUCLEAR LEUKOCYTES | CHRONIC-RENAL-FAILURE | Cell Degranulation | Oxidative Stress | Humans | Neutrophils - physiology | Cystic Fibrosis - etiology | Cell Adhesion | Animals | Bacterial Infections - immunology | Cytokines - biosynthesis | Phagocytosis | Antibodies, Antineutrophil Cytoplasmic - physiology | Apoptosis | Cell Movement
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5. Full Text Complement alternative pathway acts as a positive feedback amplification of neutrophil activation
by Camous, Laurent and Roumenina, Lubka and Bigot, Sylvain and Brachemi, Soumeya and Frémeaux-Bacchi, Véronique and Lesavre, Philippe and Halbwachs-Mecarelli, Lise
Blood, ISSN 0006-4971, 01/2011, Volume 117, Issue 4, pp. 1340 - 1349
Complement alternative pathway plays an important, but not clearly understood, role in neutrophil-mediated diseases. We here show that neutrophils themselves... 
SYSTEM | MEMBRANE ATTACK | C5A RECEPTOR | PHAGOCYTOSIS | ENDOTHELIAL-CELLS | APOPTOTIC CELLS | DECAY-ACCELERATING FACTOR | MODEL | MICROPARTICLES | HEMATOLOGY | PROPERDIN BINDS | Neutrophil Activation - immunology | Complement C5 - metabolism | Tetradecanoylphorbol Acetate - pharmacology | Complement C3 - metabolism | Humans | Neutrophils - drug effects | Blood - immunology | Cells, Cultured | Neutrophil Activation - drug effects | Neutrophils - immunology | Neutrophils - physiology | Blood - drug effects | Neutrophil Activation - physiology | N-Formylmethionine Leucyl-Phenylalanine - analogs & derivatives | Tumor Necrosis Factor-alpha - pharmacology | Complement Pathway, Alternative - drug effects | Complement Pathway, Alternative - physiology | N-Formylmethionine Leucyl-Phenylalanine - pharmacology | Feedback, Physiological - drug effects | Feedback, Physiological - physiology | Neutrophils - metabolism | Complement Activation - drug effects | Complement Activation - physiology
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6. Full Text Complement activation by heme as a secondary hit for atypical hemolytic uremic syndrome
by Frimat, Marie and Frimat, Marie and Tabarin, Fanny and Tabarin, Fanny and Dimitrov, Jordan D and Dimitrov, Jordan D and Poitou, Caroline and Poitou, Caroline and Halbwachs-Mecarelli, Lise and Halbwachs-Mecarelli, Lise and Fremeaux-Bacchi, Veronique and Fremeaux-Bacchi, Veronique and Roumenina, Lubka T and Roumenina, Lubka T
Blood, ISSN 0006-4971, 07/2013, Volume 122, Issue 2, pp. 282 - 292
Atypical hemolytic uremic syndrome (aHUS) is characterized by genetic and acquired abnormalities of the complement system leading to alternative pathway (AP)... 
HEMOGLOBIN | OXIDATIVE STRESS | OXIDANT DAMAGE | CONVERTASE | MICROVASCULAR THROMBOSIS | PATHWAY | ENDOTHELIAL-CELLS | FACTOR-H | MUTATIONS | PROTEINS | HEMATOLOGY | Cell Line | Complement C3-C5 Convertases - metabolism | Heme - metabolism | Hemolytic-Uremic Syndrome - metabolism | Complement C3 - metabolism | Endothelial Cells - metabolism | P-Selectin - metabolism | Humans | Complement Activation - immunology | Hemolytic-Uremic Syndrome - immunology | Protein Binding - immunology | Complement C3 - immunology | Endothelial Cells - immunology | Heme - immunology | Complement C3b - metabolism | Complement C3 - chemistry | Heme - chemistry | Complement Pathway, Alternative - immunology | Cell Membrane - immunology | Cell Membrane - metabolism | Mutation | Atypical Hemolytic Uremic Syndrome | Complement C3 - genetics | Complement C3b - immunology
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