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European Journal of Immunology, ISSN 0014-2980, 10/2015, Volume 45, Issue 10, pp. 2847 - 2857
The pathogenesis of inflammatory skin diseases such as psoriasis involves the release of numerous proinflammatory cytokines, including members of the IL‐1... 
IL‐1R | Skin inflammation | NLRP3 inflammasome | Imiquimod | MyD88 | IL-1R | INTERLEUKIN-1 | RECEPTOR | KERATINOCYTES | CYTOKINE | IMMUNOLOGY | IL-22 | DISEASE | DEFICIENT | ABSENCE | EXPRESSION | PSORIASIS | Adjuvants, Immunologic - pharmacology | Receptors, Interleukin-1 Type I - immunology | Drug Eruptions - pathology | NLR Family, Pyrin Domain-Containing 3 Protein | Adjuvants, Immunologic - adverse effects | Signal Transduction - immunology | Toll-Like Receptor 7 - immunology | Myeloid Differentiation Factor 88 - immunology | Membrane Glycoproteins - immunology | Aminoquinolines - pharmacology | Cytokines - genetics | Drug Eruptions - genetics | Carrier Proteins - immunology | Drug Eruptions - immunology | Skin - pathology | Cytokines - immunology | Skin - immunology | Toll-Like Receptor 7 - genetics | Myeloid Differentiation Factor 88 - genetics | Signal Transduction - genetics | Inflammasomes - genetics | Membrane Glycoproteins - genetics | Mice, Knockout | Carrier Proteins - genetics | Animals | Signal Transduction - drug effects | Inflammasomes - immunology | Receptors, Interleukin-1 Type I - genetics | Mice | Aminoquinolines - adverse effects | Skin | Inflammation | Psoriasis | RNA | Dermatitis | Rodents | Life Sciences | Human health and pathology | Immunology | Dermatology | Biochemistry, Molecular Biology | Innate immunity | Biomolecules | Adaptive immunology
Journal Article
Science, ISSN 0036-8075, 01/2018, Volume 359, Issue 6371, pp. 91 - 97
Immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis induce sustained clinical responses in a sizable minority of cancer patients. We found that... 
CELL LUNG-CANCER | MELANOMA | MICROENVIRONMENT | INTESTINAL MICROBIOTA | CYCLOPHOSPHAMIDE | PD-1 BLOCKADE | MULTIDISCIPLINARY SCIENCES | GENES | RESISTANCE | ANTITUMOR IMMUNITY | NIVOLUMAB | CD4 Antigens - immunology | Immunotherapy - methods | Humans | Antibodies, Monoclonal - therapeutic use | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Gastrointestinal Microbiome - genetics | Fecal Microbiota Transplantation | Anti-Bacterial Agents - therapeutic use | Feces - microbiology | Metagenome - genetics | Neoplasms - therapy | Animals | Receptors, CCR - immunology | Interleukin-12 - immunology | Receptors, CXCR3 - immunology | T-Lymphocytes - immunology | Mice | Gastrointestinal Microbiome - immunology | Verrucomicrobia - genetics | Verrucomicrobia - immunology | Care and treatment | Cell receptors | Microbiota (Symbiotic organisms) | Immunotherapy | Epithelial tumors | Physiological aspects | Health aspects | Methods | Apoptosis | PD-1 protein | Interleukin | Microbiomes | Transplantation | Lymphocytes T | Anticancer properties | Microbiota | Lymphocytes | Bacteria | Feces | Supplementation | Gnotobiotics | Kidneys | Melanoma | Dietary supplements | Interleukin 12 | Abundance | CXCR3 protein | Patients | CD4 antigen | Immune checkpoint | Antibiotics | Lungs | Flora | PD-L1 protein | Relative abundance | Antitumor activity | CCR9 protein | Tumors | Kidney transplantation | Cancer | Life Sciences
Journal Article
Nature, ISSN 0028-0836, 2011, Volume 474, Issue 7351, pp. 385 - 389
Live vaccines have long been known to trigger far more vigorous immune responses than their killed counterparts(1-6). This has been attributed to the ability... 
TRANSCRIPTION FACTORS | PHAGOSOME | PROTECTIVE IMMUNITY | ACTIVATION | T-CELL RESPONSES | RECOGNITION | MULTIDISCIPLINARY SCIENCES | INFLAMMASOME | TOLL-LIKE RECEPTORS | INNATE | REGULATORS | Phagosomes - microbiology | RNA, Messenger - immunology | Inflammasomes - metabolism | Interferon-beta - immunology | Bacterial Vaccines - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Dendritic Cells - immunology | Adaptor Proteins, Vesicular Transport - deficiency | Microbial Viability - immunology | Bacteria - immunology | Phagosomes - immunology | Interferon-beta - genetics | RNA, Bacterial - genetics | Macrophages - immunology | Macrophages - microbiology | Mice, Inbred C57BL | RNA, Messenger - genetics | Cells, Cultured | Microbial Viability - genetics | Adaptor Proteins, Vesicular Transport - immunology | Macrophages - cytology | Bacteria - genetics | Virulence Factors | Immunity, Innate - immunology | Vaccines, Attenuated - immunology | Vaccines, Inactivated - immunology | Animals | Carrier Proteins - metabolism | Bacterial Vaccines - immunology | Inflammasomes - immunology | Dendritic Cells - microbiology | RNA, Bacterial - immunology | Antibodies, Bacterial - immunology | Bacteria - pathogenicity | Dendritic Cells - cytology | Mice | Phagocytosis | Vaccines, Attenuated - genetics | Proteins | Bacteria | Microbiology | Kinases | Immune system | toll-like receptors | transcription factors | inflammasome | innate | recognition | phagosome | t-cell responses | activation | regulators | protective immunity
Journal Article
Nature Medicine, ISSN 1078-8956, 09/2007, Volume 13, Issue 9, pp. 1050 - 1059
Journal Article
PLoS ONE, ISSN 1932-6203, 07/2014, Volume 9, Issue 7, pp. e99383 - e99383
The exact implication of innate immunity in granuloma formation and irreversible lung fibrosis remains to be determined. In this study, we examined the lung... 
FIBROSIS | TUMOR-NECROSIS-FACTOR | INDUCED PULMONARY INFLAMMATION | NMRI MICE | INDUCED LUNG INFLAMMATION | C57BL/6 MICE | MULTIDISCIPLINARY SCIENCES | RECEPTOR ANTAGONIST | MURINE SILICOSIS | T-LYMPHOCYTES | NALP3 INFLAMMASOME | Immunohistochemistry | Inflammation - chemically induced | T-Lymphocytes, Regulatory - metabolism | Granuloma - metabolism | Interleukin-1alpha - immunology | Receptors, Interleukin-1 - genetics | Immunity, Innate - genetics | Interleukin-1alpha - metabolism | Pulmonary Fibrosis - genetics | Interleukin-1beta - genetics | Silicosis - genetics | T-Lymphocytes, Regulatory - immunology | Signal Transduction - immunology | Flow Cytometry | Th17 Cells - metabolism | Interleukin-1beta - metabolism | Myeloid Differentiation Factor 88 - immunology | Interleukin-1alpha - genetics | Cytokines - genetics | Silicosis - immunology | Cytokines - immunology | Granuloma - genetics | Silicosis - etiology | Cytokines - metabolism | Receptors, Interleukin-1 - immunology | Silicon Dioxide - immunology | Mice, Inbred C57BL | Myeloid Differentiation Factor 88 - genetics | Pulmonary Fibrosis - immunology | Interleukin-1beta - immunology | Inflammation - immunology | Signal Transduction - genetics | Mice, Knockout | Receptors, Interleukin-1 - metabolism | Immunity, Innate - immunology | Animals | Silicon Dioxide - toxicity | Inflammation - genetics | Pulmonary Fibrosis - chemically induced | Th17 Cells - immunology | Granuloma - immunology | Myeloid Differentiation Factor 88 - metabolism | Platelet-derived growth factor | Collagen | Analysis | Inflammation | T cells | Transforming growth factors | Silica | Granuloma | Collagens | Parenchyma | Inflammatory response | Innate immunity | Lymphocytes T | Interleukin 1 receptors | Kinases | Immunity | Accumulation | Silicon dioxide | Toxicology | Lymphocytes | Rodents | Interleukin 1 | Toll-like receptors | Tumor necrosis factor-TNF | Cytokines | Sarcoidosis | Lung diseases | Pharmacology | Gene expression | Pulmonary fibrosis | Lungs | TLR2 protein | Interleukin 10 | Fibrosis | MyD88 protein | TNF inhibitors | Mice | Index Medicus
Journal Article
PLoS Pathogens, ISSN 1553-7366, 05/2008, Volume 4, Issue 5, pp. e1000078 - e1000078
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2013, Volume 8, Issue 3, p. e58452
IL-17A induces the release of pro-inflammatory cytokines and of reactive oxygen species which could lead to neutrophilic inflammation. We determined the role... 
STIMULATION | INTERLEUKIN-17 | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | DISEASE | OZONE | MICE | CHEMOKINE | EXPRESSION | NEUTROPHIL RECRUITMENT | T-CELLS | Airway Resistance - drug effects | Oxidative Stress | Isometric Contraction - drug effects | Male | Receptors, Interleukin-17 - genetics | Bronchial Hyperreactivity - genetics | Bronchi - drug effects | Inflammation - metabolism | Dexamethasone - pharmacology | Bronchi - metabolism | Bronchial Hyperreactivity - metabolism | Phosphorylation - drug effects | Receptors, Interleukin-17 - metabolism | Cytokines - metabolism | Acetylcholine - pharmacology | Emphysema - metabolism | Mice, Knockout | Interleukin-17 - metabolism | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Inflammation - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Emphysema - genetics | Mitogen-Activated Protein Kinases - metabolism | Acetylcholine | Inflammation | Dexamethasone | Cytokines | Emphysema, Pulmonary | Heart | Oxidative stress | Reactive oxygen species | Smooth muscle | Respiratory tract | Signal transduction | Rodents | Chronic obstructive pulmonary disease | Neutrophils | Contractility | Muscles | MAP kinase | Ozone | Leukocytes (neutrophilic) | Exposure | Gene expression | Cigarettes | Muscle contraction | Interleukin 17 | Asthma | Signaling | Lungs | Protein kinase | Emphysema | Chemokines
Journal Article
Journal of Experimental Medicine, ISSN 0022-1007, 03/2011, Volume 208, Issue 3, pp. 491 - 503
IL-17 production by γδ T cells is required for tumor cell infiltration by IFN-γ–producing CD8 + T cells and inhibition of tumor growth in response to... 
Journal Article