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1. Full Text C1q restrains autoimmunity and viral infection by regulating CD8+ T cell metabolism
by Ling, Guang Sheng and Crawford, Greg and Buang, Norzawani and Bartok, Istvan and Tian, Kunyuan and Thielens, Nicole M and Bally, Isabelle and Harker, James A and Ashton-Rickardt, Philip G and Rutschmann, Sophie and Strid, Jessica and Botto, Marina
Science (American Association for the Advancement of Science), ISSN 0036-8075, 05/2018, Volume 360, Issue 6388, pp. 558 - 563
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Immunoglobulins - immunology | Complement C1q - physiology | Autoimmunity - genetics | Complement C1q - genetics | Lymphocytic Choriomeningitis - immunology | Complement Pathway, Classical - immunology | Autoantibodies - immunology | Animals | Autoimmunity - immunology | Mice, Mutant Strains | Lupus Erythematosus, Systemic - genetics | Lupus Erythematosus, Systemic - immunology | CD8-Positive T-Lymphocytes - metabolism | Mice | Complement C3 - genetics | Complement Pathway, Classical - genetics | Immunologic Memory - immunology | Complement C3 - physiology | Disease Models, Animal | Lymphocytic Choriomeningitis - genetics | Graft-versus-host reaction | CD8 antigen | Chronic infection | Effector cells | Complement | Lymphocytes T | Infections | Cell surface | Protein turnover | Proteins | Mitochondria | Systemic lupus erythematosus | Lymphocytes | Lupus | Antigens | Abnormalities | Autoantigens | Metabolism | Complement component C1q | Chronic conditions | Cellular biology | Complement component C3 | Autoimmune diseases | Viral infections | Classical pathway | Apoptosis | Index Medicus | Life Sciences | Biomolecules | Biochemistry, Molecular Biology
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2. Full Text RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL
by Lawlor, Kate E and Khan, Nufail and Mildenhall, Alison and Gerlic, Motti and Croker, Ben A and D'Cruz, Akshay A and Hall, Cathrine and Kaur Spall, Sukhdeep and Anderton, Holly and Masters, Seth L and Rashidi, Maryam and Wicks, Ian P and Alexander, Warren S and Mitsuuchi, Yasuhiro and Benetatos, Christopher A and Condon, Stephen M and Wong, W. Wei-Lynn and Silke, John and Vaux, David L and Vince, James E
Nature communications, ISSN 2041-1723, 02/2015, Volume 6, Issue 1, pp. 6282 - 6282
Science & Technology - Other Topics | Multidisciplinary Sciences | Science & Technology | Protein Kinases - metabolism | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Tumor Necrosis Factor-alpha - metabolism | Inflammasomes - metabolism | Bone Marrow Cells - cytology | NLR Family, Pyrin Domain-Containing 3 Protein | Autoantibodies - chemistry | Mice, Inbred C57BL | Caspase 8 - metabolism | Male | Inflammation | Liver - embryology | Necrosis | Animals | Carrier Proteins - metabolism | Interleukin-1beta - metabolism | X-Linked Inhibitor of Apoptosis Protein - metabolism | Female | Inhibitor of Apoptosis Proteins - metabolism | Lipopolysaccharides - chemistry | Mice | Enzyme Activation | Apoptosis | Index Medicus
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3. Full Text Cutting edge: CGAS is required for lethal autoimmune disease in the Trex1-deficient mouse model of Aicardi-Goutières syndrome
by Gray, Elizabeth E and Treuting, Piper M and Woodward, Joshua J and Stetson, Daniel B
The Journal of immunology (1950), ISSN 0022-1767, 09/2015, Volume 195, Issue 5, pp. 1939 - 1943
Life Sciences & Biomedicine | Immunology | Science & Technology | Nucleotides, Cyclic - metabolism | Phosphoproteins - immunology | Exodeoxyribonucleases - immunology | Interferon-beta - immunology | Nervous System Malformations - immunology | Gene Expression - drug effects | Autoantibodies - blood | Humans | Immunoblotting | Interferons - immunology | Phosphoproteins - metabolism | Inflammation - metabolism | Nervous System Malformations - metabolism | Autoimmune Diseases of the Nervous System - genetics | Gene Expression - immunology | Interferon-beta - genetics | Exodeoxyribonucleases - genetics | Nucleotidyltransferases - metabolism | Autoimmune Diseases of the Nervous System - metabolism | Nervous System Malformations - genetics | Macrophages - immunology | Disease Models, Animal | Fibroblasts - metabolism | Interferons - pharmacology | Mice, Inbred C57BL | Cells, Cultured | Inflammation - immunology | Phosphoproteins - genetics | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Autoimmune Diseases of the Nervous System - immunology | Autoantibodies - immunology | Macrophages - metabolism | Animals | Interferon-beta - metabolism | Embryo, Mammalian - cytology | Fibroblasts - drug effects | Exodeoxyribonucleases - metabolism | Inflammation - genetics | Nucleotidyltransferases - genetics | Fibroblasts - immunology | Macrophages - drug effects | Nucleotidyltransferases - immunology | Nucleotides, Cyclic - immunology | Index Medicus | Abridged Index Medicus
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4. Full Text Necrosis in anti-SRP+ and anti-HMGCR+myopathies: Role of autoantibodies and complement
by Allenbach, Yves and Arouche-Delaperche, Louiza and Preusse, Corinna and Radbruch, Helena and Butler-Browne, Gillian and Champtiaux, Nicolas and Mariampillai, Kuberaka and Rigolet, Aude and Hufnagl, Peter and Zerbe, Norman and Amelin, Damien and Maisonobe, Thierry and Louis-Leonard, Sarah and Duyckaerts, Charles and Eymard, Bruno and Goebel, Hans-Hilmar and Bergua, Cecile and Drouot, Laurent and Boyer, Olivier and Benveniste, Olivier and Stenzel, Werner
Neurology, ISSN 0028-3878, 02/2018, Volume 90, Issue 6, pp. e507 - e517
Clinical Neurology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Myofibrils - pathology | Signal Recognition Particle - metabolism | Autoantibodies - blood | Humans | Endoplasmic Reticulum - metabolism | Male | Muscle, Skeletal - metabolism | Interleukin-1beta - genetics | RNA, Messenger - metabolism | Antigens, CD - metabolism | Complement System Proteins - metabolism | Hydroxymethylglutaryl CoA Reductases - metabolism | Interleukin-1beta - metabolism | Female | Hydroxymethylglutaryl CoA Reductases - immunology | Macrophages - pathology | Muscle, Skeletal - ultrastructure | Muscular Diseases - blood | Lymphocytes - pathology | Signal Recognition Particle - immunology | Nitric Oxide Synthase Type II - genetics | Necrosis - etiology | Neural Cell Adhesion Molecules - metabolism | Muscular Diseases - complications | Myofibrils - metabolism | Muscle, Skeletal - pathology | Nitric Oxide Synthase Type II - metabolism
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5. Full Text Autoantibody-Mediated Complement C3a Receptor Activation Contributes to the Pathogenesis of Preeclampsia
by Wang, Wei and Irani, Roxanna A and Zhang, Yujin and Ramin, Susan M and Blackwell, Sean C and Tao, Lijian and Kellems, Rodney E and Xia, Yang
Hypertension (Dallas, Tex. 1979), ISSN 0194-911X, 09/2012, Volume 60, Issue 3, pp. 712 - 721
receptor | autoantibody | C3a receptor | complement C3a | placenta | preeclampsia | hypertension | Peripheral Vascular Disease | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Cardiology. Vascular system | Biological and medical sciences | Arterial hypertension. Arterial hypotension | Medical sciences | Clinical manifestations. Epidemiology. Investigative techniques. Etiology | Blood and lymphatic vessels | Autoantibodies - metabolism | Humans | Pregnancy, Animal - metabolism | Case-Control Studies | Hypertension - etiology | Receptors, Complement - metabolism | Kidney - metabolism | Adult | Female | Models, Animal | Pre-Eclampsia - metabolism | Pregnancy Complications - metabolism | Proteinuria - etiology | Pregnancy Complications - etiology | Complement C3 - metabolism | Tissue Culture Techniques | Mice, Inbred C57BL | Proteinuria - metabolism | Vascular Endothelial Growth Factor Receptor-1 - metabolism | Chorionic Villi - metabolism | Pre-Eclampsia - etiology | Hypertension - metabolism | Placenta - metabolism | Pregnancy | Animals | Receptor, Angiotensin, Type 1 - metabolism | Mice | Index Medicus | AT1 receptor
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6. Full Text Contactin-1 IgG4 antibodies cause paranode dismantling and conduction defects
by Manso, Constance and Querol, Luis and Mekaouche, Mourad and Illa, Isabel and Devaux, Jérôme J
Brain (London, England : 1878), ISSN 0006-8950, 2016, Volume 139, Issue 6, pp. 1700 - 1712
Autoantibody | Dysimmune | Neuritis | Caspr | CIDP | Neurosciences | Clinical Neurology | Neurosciences & Neurology | Life Sciences & Biomedicine | Science & Technology | Ranvier's Nodes - immunology | Autoantibodies - metabolism | Humans | Male | Nerve Growth Factors - metabolism | Cell Adhesion Molecules - immunology | Ranvier's Nodes - metabolism | Sciatic Nerve - metabolism | Immunoglobulin G - immunology | Contactin 1 - metabolism | Cell Adhesion Molecules, Neuronal - metabolism | Membrane Proteins - metabolism | Nerve Tissue Proteins - immunology | Rats | Membrane Proteins - immunology | Neural Conduction - physiology | Nerve Growth Factors - immunology | Cell Adhesion Molecules - metabolism | Nerve Tissue Proteins - metabolism | Autoantibodies - immunology | Animals | Contactin 1 - immunology | Neural Conduction - immunology | Cell Adhesion Molecules, Neuronal - immunology | Immunoglobulin G - metabolism | Index Medicus | Abridged Index Medicus
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7. Full Text Self-reactive IgE exacerbates interferon responses associated with autoimmunity
by Henault, Jill and Riggs, Jeffrey M and Karnell, Jodi L and Liarski, Vladimir M and Li, Jianqing and Shirinian, Lena and Xu, Linda and Casey, Kerry A and Smith, Michael A and Khatry, Deepak B and Izhak, Liat and Clarke, Lorraine and Herbst, Ronald and Ettinger, Rachel and Petri, Michelle and Clark, Marcus R and Mustelin, Tomas and Kolbeck, Roland and Sanjuan, Miguel A
Nature immunology, ISSN 1529-2908, 02/2016, Volume 17, Issue 2, pp. 196 - 203
Life Sciences & Biomedicine | Immunology | Science & Technology | Autoimmunity | Leukocytes, Mononuclear - metabolism | Immunoglobulin G - blood | Antibodies, Antinuclear - immunology | Dendritic Cells - immunology | Humans | Interferons - secretion | Lupus Erythematosus, Systemic - metabolism | Male | Lupus Erythematosus, Systemic - blood | Immunoglobulin E - blood | Immunoglobulin E - immunology | Immunoglobulin G - immunology | Leukocytes, Mononuclear - immunology | Lupus Erythematosus, Systemic - immunology | Female | Plasma Cells - metabolism | Antigen-Antibody Complex - metabolism | B-Lymphocytes - metabolism | Dendritic Cells - metabolism | Cytokines - blood | Lupus Nephritis - pathology | Cytokines - metabolism | Phagosomes - metabolism | Phagocytosis - immunology | Lupus Nephritis - immunology | Autoantibodies - immunology | B-Lymphocytes - immunology | Interferons - metabolism | Antigen-Antibody Complex - immunology | Toll-Like Receptor 9 - metabolism | Plasma Cells - immunology | Complications and side effects | Care and treatment | Systemic lupus erythematosus | Immunoglobulin E | Influence | Interferon | Research | Index Medicus
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8. Full Text IgM rheumatoid factor amplifies the inflammatory response of macrophages induced by the rheumatoid arthritis-specific immune complexes containing anticitrullinated protein antibodies
by Laurent, Lætitia and Anquetil, Florence and Clavel, Cyril and Ndongo-Thiam, Ndiémé and Offer, Géraldine and Miossec, Pierre and Pasquali, Jean-Louis and Sebbag, Mireille and Serre, Guy
Annals of the rheumatic diseases, ISSN 0003-4967, 07/2015, Volume 74, Issue 7, pp. 1425 - 1431
Life Sciences & Biomedicine | Rheumatology | Science & Technology | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Humans | Rheumatoid Factor - pharmacology | Synovial Membrane - pathology | Synovial Membrane - drug effects | Case-Control Studies | Antibodies, Anti-Idiotypic - metabolism | Immunoglobulin M - metabolism | Arthritis, Rheumatoid - metabolism | Inflammation - metabolism | Antigen-Antibody Complex - metabolism | Severity of Illness Index | Cytokines - metabolism | Macrophages - pathology | Cells, Cultured | Rheumatoid Factor - metabolism | Peptides, Cyclic - immunology | Synovial Membrane - metabolism | Arthritis, Rheumatoid - pathology | Macrophages - metabolism | Macrophages - drug effects | In Vitro Techniques | Immunoglobulin G - metabolism | Immunoglobulin M - pharmacology | Immunoglobulin M | Autoantibodies | Immune response | Rheumatoid arthritis | Analysis | Research | Risk factors | Proteins | Studies | Hypotheses | Disease | Cytokines | Tumor necrosis factor-TNF | Binding sites | Index Medicus
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9. Full Text Ion channelopathies of the immune system
by Vaeth, Martin and Feske, Stefan
Current opinion in immunology, ISSN 0952-7915, 06/2018, Volume 52, pp. 39 - 50
Life Sciences & Biomedicine | Immunology | Science & Technology | Infections - metabolism | Infections - complications | Calcium Release Activated Calcium Channels - genetics | Humans | Channelopathies - immunology | Ion Channels - genetics | Channelopathies - metabolism | Stromal Interaction Molecule 1 - genetics | Agammaglobulinemia - metabolism | Cation Transport Proteins - metabolism | Immune System - immunology | Cation Transport Proteins - genetics | Calcium Release Activated Calcium Channels - metabolism | Infections - immunology | ORAI1 Protein - metabolism | Disease Susceptibility | ORAI1 Protein - genetics | Channelopathies - etiology | Agammaglobulinemia - etiology | Carrier Proteins - genetics | Stromal Interaction Molecule 1 - metabolism | Autoantibodies - immunology | Animals | Carrier Proteins - metabolism | Ion Channels - metabolism | Immune System - metabolism | Zinc - deficiency | Proteins | Autoimmunity | Zinc compounds | Medical colleges | Autoantibodies | Disease susceptibility | Immune system | Index Medicus
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