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PLoS ONE, ISSN 1932-6203, 08/2011, Volume 6, Issue 8, p. e23989
Toll-like receptors (TLRs) activate a potent immunostimulatory response. There is clear evidence that overactivation of TLRs leads to infectious and... 
STRUCTURAL BASIS | CRYSTAL-STRUCTURE | PROTEIN-DOCKING | MULTIDISCIPLINARY SCIENCES | ENDOTOXIN TOLERANCE | TIR-DOMAIN | INTERLEUKIN-1 RECEPTOR | IL-1 RECEPTOR | MYD88 ADAPTER-LIKE | QUALITY ASSESSMENT | INNATE IMMUNITY | Interleukin-1 Receptor-Like 1 Protein | Humans | Protein Multimerization | Proteolipids - metabolism | Molecular Sequence Data | Myeloid Differentiation Factor 88 - chemistry | Myelin and Lymphocyte-Associated Proteolipid Proteins | Protein Structure, Quaternary | Membrane Transport Proteins - metabolism | Receptors, Cell Surface - chemistry | Protein Stability | Protein Structure, Tertiary | Toll-Like Receptor 6 - metabolism | Amino Acid Sequence | Toll-Like Receptor 6 - chemistry | Signal Transduction | Computational Biology | Receptors, Cell Surface - metabolism | Toll-Like Receptor 4 - chemistry | Toll-Like Receptor 2 - metabolism | Toll-Like Receptor 4 - metabolism | Molecular Dynamics Simulation | Membrane Transport Proteins - chemistry | Myelin Proteins - chemistry | Sequence Alignment | Myelin Proteins - metabolism | Myeloid Differentiation Factor 88 - metabolism | Toll-Like Receptor 2 - chemistry | Proteolipids - chemistry | Molecular dynamics | Medicine, Experimental | Medical research | Structure | Analysis | Crystals | Nuclear magnetic resonance--NMR | Genes | Science | Homology | Innate immunity | Interleukin 1 receptors | Kinases | Immunity | Inflammatory diseases | Molecular docking | Proteins | Signal transduction | Receptors | Pathways | Hydrogen bonds | Rodents | Interleukin 1 | Toll-like receptors | Trends | Inhibition | Crystal structure | Immune system | Immunostimulation | Cytokines | Computer simulation | Adapters | TLR4 protein | Signaling | Molecular modelling | TLR1 protein | TLR2 protein | MyD88 protein | Ligands | In vivo methods and tests | Regulation | Mutation | Three dimensional models | Nuclear magnetic resonance | NMR
Journal Article
Cellular Microbiology, ISSN 1462-5814, 11/2010, Volume 12, Issue 11, pp. 1648 - 1665
Summary In human monocytes, Toll‐like receptor (TLR) 2/1 activation leads to vitamin D3‐dependent antimycobacterial activities, but the molecular mechanisms by... 
CELLS | INNATE IMMUNE-RESPONSES | PATHWAY | PROTEIN-KINASE | HUMAN MACROPHAGES | TUBERCULOSIS | TOLL-LIKE RECEPTORS | MICROBIOLOGY | ANTIVIRAL IMMUNITY | HUMAN MONOCYTES | TLR2 | CELL BIOLOGY | Monocytes - microbiology | AMP-Activated Protein Kinases - metabolism | Calcium | Signal Transduction | Lipoproteins - genetics | Humans | Toll-Like Receptor 1 - metabolism | Bacterial Proteins - genetics | Cells, Cultured | 25-Hydroxyvitamin D3 1-alpha-Hydroxylase - metabolism | Receptors, Calcitriol - metabolism | Toll-Like Receptor 2 - metabolism | Antimicrobial Cationic Peptides - metabolism | Autophagy | CCAAT-Enhancer-Binding Protein-beta - metabolism | Lipopolysaccharide Receptors - metabolism | Mycobacterium tuberculosis | Lipoproteins - metabolism | Bacterial Proteins - metabolism | Vitamin D - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Antimicrobial Cationic Peptides - genetics | Monocytes - physiology | Medical colleges | Vitamin D | Cytochrome P-450 | Calcifediol | Protein C | Alfacalcidol | Protein kinases | Antibacterial agents | Antimicrobial activity | Calcium (intracellular) | cathelicidins | Hydroxylase | Data processing | MAP kinase | CCAAT/enhancer-binding protein | AMP-activated protein kinase | CD14 antigen | Signal transduction | Cell activation | Lipoproteins | Monocytes | Molecular modelling | TLR2 protein | Toll-like receptors | Vitamin D receptors | Phagocytosis
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 07/2001, Volume 98, Issue 15, pp. 8774 - 8779
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2013, Volume 8, Issue 5, p. e63793
Hepatitis E virus (HEV) is a major cause of enterically transmitted acute hepatitis in developing nations and occurs in sporadic and epidemic forms. The... 
PATHWAYS | CYTOKINE PRODUCTION | ORF3 PROTEIN | UBIQUITIN LIGASE | INNATE IMMUNE RECEPTORS | MULTIDISCIPLINARY SCIENCES | HEV | HEPATOMA-CELLS | C VIRUS | PATTERN-RECOGNITION RECEPTORS | EXPRESSION | Epithelial Cells - metabolism | Hepatitis E - genetics | Humans | Adaptor Proteins, Vesicular Transport - genetics | NF-kappa B - immunology | NF-kappa B - metabolism | Hepatitis E - metabolism | Transcriptome - immunology | Adaptor Proteins, Vesicular Transport - metabolism | Interferon Regulatory Factor-3 - genetics | Host-Pathogen Interactions - immunology | Hepatitis E virus - immunology | RNA Interference | Hepatitis E - immunology | Myeloid Differentiation Factor 88 - immunology | Capsid Proteins - immunology | Cytokines - genetics | Chemokines - immunology | Cytokines - immunology | Interferon Regulatory Factor-3 - immunology | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Myeloid Differentiation Factor 88 - genetics | Virus Replication - immunology | Transcriptome - genetics | Adaptor Proteins, Vesicular Transport - immunology | Reverse Transcriptase Polymerase Chain Reaction | Chemokines - genetics | Blotting, Western | Hepatitis E virus - physiology | NF-kappa B - genetics | Epithelial Cells - immunology | Epithelial Cells - virology | Cell Line, Tumor | Interferon Regulatory Factor-3 - metabolism | Chemokines - metabolism | Myeloid Differentiation Factor 88 - metabolism | Medical research | Hepatitis E | Genes | Development and progression | DNA binding proteins | Genetic transcription | Biological response modifiers | Infection | Disease transmission | Viral proteins | Tumor necrosis factor | Medicine, Experimental | Interferon | Health aspects | Cell culture | Post-transcription | Epidemics | Transcription factors | Capsid protein | Pathogenesis | Epithelial cells | RANTES | Gene regulation | Inflammatory response | Viruses | Genomes | Infections | Developing countries--LDCs | Interleukin 6 | Proteins | DNA helicase | Hepatitis | Reporter gene | Rodents | Toll-like receptors | Interleukin 8 | Immune system | Adaptor proteins | NF-κB protein | Immune response | Cytokines | Inflammation | Adaptors | Gene expression | TLR3 protein | Virology | Pregnancy | Molecular modelling | Interferon regulatory factor 3 | Lungs | TLR2 protein | Influenza | MyD88 protein | Human behavior | Protein structure | Chemokines | Viral infections | Developing countries | Developing nations
Journal Article
Cell Death and Disease, ISSN 2041-4889, 2017, Volume 8, Issue 5, pp. e2763 - e2763
Sepsis is a systemic inflammation caused by infection. The balance between M1-M2 macrophage polarization has an essential role in the pathogenesis of sepsis.... 
ACUTE KIDNEY INJURY | REGULATOR | M2 MACROPHAGES | RECEPTOR 2 | INFLAMMATION | DIFFERENTIATION | MAPK | NF-KAPPA-B | CBL-B | MASL1 | CELL BIOLOGY | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Oncogene Proteins - genetics | Lipopeptides - pharmacology | Humans | Tumor Necrosis Factor-alpha - genetics | JNK Mitogen-Activated Protein Kinases - metabolism | Cell Cycle Proteins - chemistry | DNA-Binding Proteins - metabolism | Inflammation - metabolism | Ubiquitination - drug effects | HEK293 Cells | Cell Cycle Proteins - genetics | Cell Polarity - drug effects | p38 Mitogen-Activated Protein Kinases - metabolism | Interleukin-6 - metabolism | Interleukin-6 - genetics | Oncogene Proteins - chemistry | Cell Cycle Proteins - metabolism | Oncogene Proteins - metabolism | Ubiquitin-Protein Ligases - metabolism | Imidazoles - pharmacology | Macrophages - cytology | Toll-Like Receptor 2 - metabolism | DNA-Binding Proteins - genetics | Ubiquitin-Protein Ligases - chemistry | DNA-Binding Proteins - chemistry | Macrophages - metabolism | Animals | Nitric Oxide Synthase Type II - genetics | Signal Transduction - drug effects | Macrophages - drug effects | RAW 264.7 Cells | Mice | Pyridines - pharmacology | Nitric Oxide Synthase Type II - metabolism | Ubiquitin | Polarization | Transcription factors | Transformation | Immunoprecipitation | Pathogenesis | c-Jun protein | Inflammation | Macrophages | Histiocytoma | Signal transduction | TLR2 protein | Toll-like receptors | Sepsis | Ubiquitin-protein ligase
Journal Article
PLoS ONE, ISSN 1932-6203, 2010, Volume 5, Issue 7, p. e11465
Background: Thymocyte expressed molecule involved in selection 1 (Themis1, SwissProt accession number Q8BGW0) is the recently characterised founder member of a... 
TUMOR-NECROSIS-FACTOR | BRUTONS TYROSINE KINASE | RICH ELEMENT | ACTIVATED PROTEIN-KINASE | POSITIVE SELECTION | MULTIDISCIPLINARY SCIENCES | MESSENGER-RNA STABILITY | MEMBRANE-PROTEINS | TNF-ALPHA PRODUCTION | NF-KAPPA-B | CANCER CELL-LINES | Immunoprecipitation | Proto-Oncogene Proteins c-vav - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Tandem Mass Spectrometry | RNA Interference | GRB2 Adaptor Protein - genetics | Toll-Like Receptors - metabolism | Intracellular Signaling Peptides and Proteins - genetics | Cell Line | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Mice, Inbred C57BL | Signal Transduction - genetics | Toll-Like Receptor 4 - metabolism | Tumor Necrosis Factor-alpha | Proteins - genetics | Animals | Proteins - metabolism | Signal Transduction - drug effects | Toll-Like Receptors - genetics | Lipopolysaccharides - pharmacology | Protein Binding | Mice | GRB2 Adaptor Protein - metabolism | Proto-Oncogene Proteins c-vav - metabolism | Tyrosine | B cells | Cytokines | RNA | Macrophages | Phosphotransferases | Osteoprogenitor cells | Biotechnology | Phosphorylation | Proline | Infections | Activation | Kinases | Guanine | Lipopolysaccharides | Interleukin 6 | Proteins | Signal transduction | Cell growth | Toll-like receptors | Bone marrow | Tumor necrosis factor-TNF | Guanine nucleotide exchange factor | Growth factors | Immune system | Pathogens | NF-κB protein | Immunoglobulins | Rheumatology | Extracellular signal-regulated kinase | JNK protein | Inflammation | Gene expression | Ribonucleic acid--RNA | TLR3 protein | Grb2 protein | Signaling | Protein arrays | Overexpression | Mutagenesis | Lymphocytes B | Interferon regulatory factor 3 | Tumor necrosis factor | Plasmids | TLR2 protein | Interferon | Cyclooxygenase-2 | Ribonucleic acid
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2016, Volume 11, Issue 4, p. e0151967
Highly purified outer membrane vesicles (OMVs) of the periodontal pathogens, Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia were... 
PROTEINASE-ADHESIN COMPLEXES | BACTEROIDES-GINGIVALIS | BACTERIA | TREPONEMA-DENTICOLA | EPITHELIAL-CELLS | SOLUBLE PEPTIDOGLYCAN | PORPHYROMONAS-GINGIVALIS | DNA | MULTIDISCIPLINARY SCIENCES | RELEASE | VIRULENCE | Cell Line | Receptors, Pattern Recognition - isolation & purification | Bacterial Outer Membrane Proteins - immunology | Bacteroides - chemistry | Receptors, Pattern Recognition - immunology | Receptors, Pattern Recognition - chemistry | Bacteroides - immunology | Humans | Treponema denticola - immunology | Bacterial Outer Membrane Proteins - chemistry | Nod2 Signaling Adaptor Protein - immunology | Porphyromonas gingivalis - chemistry | Toll-Like Receptor 4 - immunology | Nod1 Signaling Adaptor Protein - immunology | Bacterial Outer Membrane Proteins - isolation & purification | Treponema denticola - chemistry | Chronic Periodontitis - microbiology | Lipopolysaccharides - analysis | Chronic Periodontitis - immunology | Toll-Like Receptor 2 - immunology | Peptidoglycan - analysis | Porphyromonas gingivalis - immunology | Virulence (Microbiology) | Periodontitis | Analysis | Risk factors | Pattern recognition receptors | Cell culture | Dental schools | Disease | Lipids | Ultracentrifugation | Nanoparticles | Proteins | Signal transduction | Receptors | Vesicles | Ultrafiltration | Rodents | Toll-like receptors | Bacteria | Nod1 protein | Deoxyribonucleic acid--DNA | NOD2 protein | Pathogens | Enzymes | Enumeration | TLR7 protein | Light scattering | Peptidoglycans | Membrane vesicles | Inflammation | Nucleic acids | Pattern recognition | TLR4 protein | Fatty acids | TLR9 protein | Cytometry | Biofilms | Oral hygiene | TLR2 protein | Deoxyribonucleic acid
Journal Article
Immunology, ISSN 0019-2805, 09/2017, Volume 152, Issue 1, pp. 138 - 149
Summary The Toll‐like receptor (TLR) adaptor proteins myeloid differentiating factor 88 (MyD88) and Toll, interleukin‐1 receptor and resistance protein (TIR)... 
T helper type 2 | Toll‐like receptor 4 | inducible co‐stimulator | Toll, interleukin‐1R and resistance protein (TIR) domain‐containing adaptor inducing interferon‐β | Asthma | inducible co-stimulator | Toll, interleukin-1R and resistance protein (TIR) domain-containing adaptor inducing interferon-β | Toll-like receptor 4 | DUST MITE ALLERGEN | TH2 RESPONSES | DENDRITIC CELLS | HELPER-CELLS | IMMUNOLOGY | RECEPTOR 4 | MONOPHOSPHORYL-LIPID-A | interleukin-1R and resistance protein (TIR) domain-containing adaptor inducing interferon | IN-VIVO | REGULATORY T-CELLS | AIRWAY HYPERRESPONSIVENESS | Toll | NF-KAPPA-B | Chemotaxis, Leukocyte | Rhinitis, Allergic, Seasonal - physiopathology | Asthma - metabolism | Cell Proliferation | Asthma - prevention & control | Bronchial Hyperreactivity - immunology | Rhinitis, Allergic, Seasonal - metabolism | Adaptor Proteins, Vesicular Transport - genetics | Adoptive Transfer | Pollen - immunology | Adaptor Proteins, Vesicular Transport - metabolism | Lipopolysaccharides - immunology | Rhinitis, Allergic, Seasonal - immunology | CD4-Positive T-Lymphocytes - immunology | Bronchoconstriction | Time Factors | Bronchial Hyperreactivity - physiopathology | Asthma - immunology | Bronchial Hyperreactivity - metabolism | Female | Lung - metabolism | Inducible T-Cell Co-Stimulator Protein - immunology | Disease Models, Animal | Genetic Predisposition to Disease | Asthma - physiopathology | Signal Transduction | Lymphocyte Activation | Mice, Inbred C57BL | CD4-Positive T-Lymphocytes - metabolism | Myeloid Differentiation Factor 88 - genetics | Antigens, Plant - immunology | Lung - physiopathology | Toll-Like Receptor 4 - immunology | Adaptor Proteins, Vesicular Transport - immunology | Bronchial Hyperreactivity - prevention & control | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Rhinitis, Allergic, Seasonal - prevention & control | Phenotype | Animals | CD4-Positive T-Lymphocytes - transplantation | Betula - immunology | Mice, Inbred BALB C | Inducible T-Cell Co-Stimulator Protein - metabolism | Cysteine Endopeptidases - immunology | Myeloid Differentiation Factor 88 - metabolism | Drug Combinations | Lung - immunology | Development and progression | Interferon | Interleukins | Biological response modifiers | T cells | β-Interferon | Mucosa | Interleukin | Stimulation | Lymphocytes T | Adoptive transfer | Lymph nodes | Recruitment | Proteins | Signal transduction | Lymphocytes | Interleukin 1 | Toll-like receptors | Foxp3 protein | Respiratory tract diseases | Pollen | Inhibition | Immune system | Adaptor proteins | Limbs | Lymphatic system | Data processing | T cell receptors | TLR4 protein | Adaptors | CD4 antigen | Drainage | Signaling | Lungs | TLR2 protein | ICOS protein | MyD88 protein | Lymph | Original
Journal Article