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Gastroenterology, ISSN 0016-5085, 04/2018, Volume 154, Issue 5, pp. 1449 - 1464.e20
The innate immune system responds not only to bacterial signals, but also to non-infectious danger-associated molecular patterns that activate the NLRP3... 
Immune Regulation | Acute Liver Failure | Biological Clock | Rev-erbα | ACUTE LIVER-FAILURE | IMMUNITY | ACTIVATION | MACROPHAGES | BEHAVIOR | Rev-erb alpha | TRANSCRIPTION | METABOLISM | REV-ERB-ALPHA | GASTROENTEROLOGY & HEPATOLOGY | CLOCK | EXPRESSION | Liver - pathology | Inflammasomes - metabolism | Macrophages, Peritoneal - pathology | Caspase 1 - metabolism | Lipopolysaccharides | Pyrrolidines - pharmacology | NLR Family, Pyrin Domain-Containing 3 Protein - genetics | Liver - immunology | Transfection | Liver - drug effects | RNA Interference | Time Factors | Peritonitis - prevention & control | Nuclear Receptor Subfamily 1, Group D, Member 1 - deficiency | Liver Failure, Acute - prevention & control | Chemical and Drug Induced Liver Injury - pathology | Macrophages, Peritoneal - drug effects | Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism | Disease Models, Animal | Galactosamine | Severity of Illness Index | Chemical and Drug Induced Liver Injury - prevention & control | Genetic Predisposition to Disease | Nuclear Receptor Subfamily 1, Group D, Member 1 - agonists | Nuclear Receptor Subfamily 1, Group D, Member 1 - genetics | Cytokines - metabolism | Signal Transduction | NLR Family, Pyrin Domain-Containing 3 Protein - metabolism | Liver - metabolism | Peritonitis - metabolism | Cells, Cultured | Macrophages, Peritoneal - immunology | Thiophenes - pharmacology | Liver Failure, Acute - metabolism | Peritonitis - immunology | Circadian Rhythm | Inflammasomes - genetics | Chemical and Drug Induced Liver Injury - immunology | Macrophage Activation | Mice, Knockout | Phenotype | Animals | Chemical and Drug Induced Liver Injury - metabolism | Inflammasomes - immunology | Liver Failure, Acute - immunology | Liver Failure, Acute - pathology | Macrophages, Peritoneal - metabolism | Hepatitis | Mitogens | Analysis | Liver | Life Sciences | Human health and pathology | rev-erb-alpha | biological clock | acute liver failure | immune regulation
Journal Article
Nature Immunology, ISSN 1529-2908, 01/2014, Volume 15, Issue 1, pp. 80 - 87
Journal Article
Science-Business eXchange, ISSN 1945-3477, 04/2009, Volume 2, Issue 17, pp. 720 - 720
Journal Article
Science-Business eXchange, ISSN 1945-3477, 06/2013, Volume 6, Issue 23, pp. 573 - 573
Journal Article
Science-Business eXchange, ISSN 1945-3477, 06/2011, Volume 4, Issue 23, pp. 657 - 657
Journal Article
Science-Business eXchange, ISSN 1945-3477, 05/2013, Volume 6, Issue 20, pp. 496 - 496
Journal Article
Science-Business eXchange, ISSN 1945-3477, 07/2011, Volume 4, Issue 28, pp. 806 - 806
Journal Article
Science-Business eXchange, ISSN 1945-3477, 10/2011, Volume 4, Issue 39, pp. 1088 - 1088
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 2015, Volume 212, Issue 10, pp. 1623 - 1640
Regulatory T (T reg) cells are central mediators of immune suppression. As such, T reg cells are characterized by a distinct pattern of gene expression, which... 
B-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | TRANSCRIPTION FACTOR FOXP3 | HELPER-CELLS | IN-VIVO | GENE-EXPRESSION | GENERATION | DIFFERENTIATION | IMMUNOLOGY | AUTOIMMUNE-DISEASE | PLASTICITY | Forkhead Transcription Factors - immunology | Receptors, Steroid - metabolism | Nuclear Receptor Subfamily 4, Group A, Member 2 - immunology | Th2 Cells - immunology | Nuclear Receptor Subfamily 4, Group A, Member 1 - immunology | Nuclear Receptor Subfamily 4, Group A, Member 2 - genetics | T-Lymphocytes, Regulatory - immunology | DNA-Binding Proteins - metabolism | Receptors, Thyroid Hormone - genetics | Forkhead Transcription Factors - metabolism | T-Lymphocytes, Helper-Inducer - immunology | Transcription, Genetic | Interleukin-4 - genetics | Receptors, Thyroid Hormone - immunology | Carrier Proteins - immunology | Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics | DNA-Binding Proteins - immunology | Nerve Tissue Proteins - immunology | Interleukin-4 - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | DNA-Binding Proteins - genetics | Forkhead Transcription Factors - genetics | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Receptors, Thyroid Hormone - metabolism | Carrier Proteins - genetics | Receptors, Steroid - immunology | Animals | Carrier Proteins - metabolism | Receptors, Steroid - genetics | Nuclear Receptor Subfamily 4, Group A, Member 1 - metabolism | Nuclear Receptor Subfamily 4, Group A, Member 2 - metabolism
Journal Article
Nature Immunology, ISSN 1529-2908, 12/2015, Volume 16, Issue 12, pp. 1228 - 1234
The molecular mechanisms that link the sympathetic stress response and inflammation remain obscure. Here we found that the transcription factor Nr4a1 regulated... 
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | NGFI-B | PRAZOSIN TREATMENT | MULTIPLE-SCLEROSIS | CELL-DEVELOPMENT | GENE-EXPRESSION | CENTRAL-NERVOUS-SYSTEM | IMMUNOLOGY | BLOOD-BRAIN-BARRIER | LEWIS RAT | NUCLEAR RECEPTOR | Tyrosine 3-Monooxygenase - metabolism | Central Nervous System - metabolism | Encephalomyelitis, Autoimmune, Experimental - metabolism | Norepinephrine - immunology | Humans | Encephalomyelitis, Autoimmune, Experimental - immunology | Nuclear Receptor Subfamily 4, Group A, Member 1 - immunology | Sympathetic Nervous System - immunology | Sympathetic Nervous System - metabolism | Central Nervous System - immunology | Inflammation - metabolism | Tyrosine 3-Monooxygenase - immunology | Myeloid Cells - immunology | Gene Expression - immunology | Encephalomyelitis, Autoimmune, Experimental - genetics | Macrophages - immunology | Disease Models, Animal | Cell Line | Rabbits | Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics | Mice, Inbred C57BL | Cells, Cultured | Inflammation - immunology | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Microscopy, Confocal | Tyrosine 3-Monooxygenase - genetics | Macrophages - metabolism | Animals | Norepinephrine - metabolism | Inflammation - genetics | Multiple Sclerosis - immunology | Multiple Sclerosis - pathology | Myeloid Cells - metabolism | Nuclear Receptor Subfamily 4, Group A, Member 1 - metabolism | Transcription factors | Immune response | Encephalomyelitis | Development and progression | Genetic aspects | Properties | Macrophages | Noradrenaline
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2013, Volume 110, Issue 12, pp. 4679 - 4684
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 08/2018, Volume 115, Issue 34, pp. E8017 - E8026
Journal Article
FASEB Journal, ISSN 0892-6638, 01/2018, Volume 32, Issue 1, pp. 254 - 264
Phagocytosis after myocardial infarction (MI) is a prerequisite to cardiac repair. Recruited monocytes clear necrotic cardiomyocytes and differentiate into... 
Myocardial infarction | Monocyte | Inflammation | TYROSINE KINASE | NUCLEAR RECEPTORS | MACROPHAGES | BIOCHEMISTRY & MOLECULAR BIOLOGY | myocardial infarction | MONOCYTES | CELL BIOLOGY | HEART-DISEASE | IN-VITRO | inflammation | APOPTOTIC CELLS | FATTY-ACID | BIOLOGY | CARDIOVASCULAR-DISEASE | monocyte | Myocardial Infarction - genetics | CD36 Antigens - deficiency | CD36 Antigens - genetics | Myocytes, Cardiac - immunology | Humans | Cardiac Output | Male | Nuclear Receptor Subfamily 4, Group A, Member 1 - immunology | Heart Rupture, Post-Infarction - etiology | Myocardial Infarction - immunology | Heart Rupture, Post-Infarction - immunology | Myocardial Infarction - pathology | Female | Macrophages - immunology | c-Mer Tyrosine Kinase - genetics | Nuclear Receptor Subfamily 4, Group A, Member 1 - agonists | Nuclear Receptor Subfamily 4, Group A, Member 1 - genetics | Macrophages - pathology | c-Mer Tyrosine Kinase - metabolism | Mice, Inbred C57BL | Cells, Cultured | Phagocytosis - immunology | CD36 Antigens - immunology | Immunity, Innate | Mice, Knockout | Myocytes, Cardiac - pathology | Animals | Apoptosis - immunology | Mice | Heart Rupture, Post-Infarction - pathology | Heart | Cell survival | Rupture | MERTK gene | Parenchyma | Cardiomyocytes | Regulatory sequences | CD36 antigen | Macrophages | Gene expression | Mitigation | Phagocytes | Monocytes | Receptors | Rodents | Bone marrow | Receptor density | Infarction | Repair | Heart diseases | Phagocytosis | Apoptosis | Research
Journal Article