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1. Full Text Abnormal CD161+ immune cells and retinoic acid receptor–related orphan receptor γt–mediate enhanced IL-17F expression in the setting of genetic hypertension
by Singh, Madhu V and Cicha, Michael Z and Kumar, Santosh and Meyerholz, David K and Irani, Kaikobad and Chapleau, Mark W and Abboud, François M
The Journal of Allergy and Clinical Immunology, ISSN 0091-6749, 09/2017, Volume 140, Issue 3, pp. 809 - 821.e3
Hypertension is considered an immunologic disorder. However, the role of the IL-17 family in genetic hypertension in the spontaneously hypertensive rat (SHR)... 
Hypertension | CD161 | IL-17 | spontaneously hypertensive rat | digoxin | T cells | retinoic acid receptor–related orphan receptor γt | TH17 | Toll-like receptor | gene expression | innate immune system | T | 17 | INTERLEUKIN 17 | ACTIVATION | ENDOTHELIAL DYSFUNCTION | ORGAN DAMAGE | IMMUNOLOGY | NICOTINIC ACETYLCHOLINE-RECEPTORS | RESPONSES | ALLERGY | INFLAMMATION | T(H)17 | retinoic acid receptor-related orphan receptor gamma t | DIFFERENTIATION | TH17 CELLS | LYMPHOCYTES | Animals, Newborn | Rats, Inbred SHR | Nuclear Receptor Subfamily 1, Group F, Member 3 - immunology | Nuclear Receptor Subfamily 1, Group F, Member 3 - antagonists & inhibitors | Poly I-C - pharmacology | Cells, Cultured | Interleukin-17 - immunology | Interleukin-17 - physiology | Interleukin-17 - genetics | Rats, Inbred WKY | Male | Hypertension - immunology | Spleen - cytology | Toll-Like Receptor 3 - agonists | NK Cell Lectin-Like Receptor Subfamily B - immunology | Digoxin - pharmacology | Hypertension - physiopathology | Vasodilation | Aging - immunology | Animals | Aorta, Thoracic - physiology | Blood Pressure - drug effects | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | RNA - metabolism | Flow cytometry | Transcription factors | Digoxin | Disease | Helper cells | Nervous system | Lymphocytes T | Birth | Kinases | Signal transduction | Splenocytes | Lymphocytes | Rodents | Measurement methods | Blood pressure | Immune system | Spleen | Immune response | Cytokines | Rats | Pharmacology | Inflammation | T cell receptors | Interleukin 17 | Endothelium | Immune systems | Acids | Prostate | Surface markers | Retinoic acid | Nicotine | Index Medicus | Abridged Index Medicus
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2. Full Text The mannose receptor negatively modulates the Toll-like receptor 4–aryl hydrocarbon receptor–indoleamine 2,3-dioxygenase axis in dendritic cells affecting T helper cell polarization
by Salazar, Fabián, MSc and Hall, Laurence, BSc and Negm, Ola H., PhD and Awuah, Dennis, MSc and Tighe, Patrick J., PhD and Shakib, Farouk, PhD, FRCPath and Ghaemmaghami, Amir M., MD, PhD
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2015, Volume 137, Issue 6, pp. 1841 - 1851.e2
Background Dendritic cells (DCs) are key players in the induction and re-elicitation of TH 2 responses to allergens. We have previously shown that different... 
Allergy and Immunology | aryl-hydrocarbon receptor | nuclear factor κB | Dendritic cells | Toll-like receptor 4 | allergy | C-type lectin receptor | indoleamine 2,3-dioxygenase | mannose receptor | TH2 | 2 | T | nuclear factor kappa B | EXPERIMENTAL ASTHMA | IDO ACTIVITY | IMMUNOLOGY | HOUSE-DUST MITE | HUMAN MONOCYTES | T(H)2 | IN-VITRO | NONINTEGRIN DC-SIGN | CYTOKINE PRODUCTION | ALLERGIC SENSITIZATION | MOUSE MODEL | NF-KAPPA-B | Indoleamine-Pyrrole 2,3,-Dioxygenase - metabolism | Mannose-Binding Lectins - metabolism | T-Lymphocytes, Helper-Inducer - metabolism | Cytokines - metabolism | Signal Transduction | Monocytes - cytology | Dendritic Cells - immunology | Humans | Receptors, Cell Surface - metabolism | Monocytes - metabolism | Gene Expression Profiling | Monocytes - immunology | Toll-Like Receptor 4 - metabolism | Lectins, C-Type - metabolism | Lymphocyte Activation - immunology | Allergens - immunology | T-Lymphocytes, Helper-Inducer - immunology | Receptors, Aryl Hydrocarbon - metabolism | Toll-Like Receptor 4 - agonists | Ligands | Dendritic Cells - metabolism | Cluster Analysis | Interleukin-12 - biosynthesis | Allergens | Allergy | Lectins | Allergic reaction | Sugars | Monosaccharides | Immunoglobulins | Transcription factors | Metabolites | Cloning | Hydrocarbons | Kinases | Allergies | Asthma | Index Medicus | Abridged Index Medicus
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3. Full Text Trim13 potentiates toll-like receptor 2-mediated nuclear factor κb activation via K29-linked polyubiquitination of tumor necrosis factor receptor-associated factor 6
by Huang, Bin and Baek, Suk-Hwan
Molecular Pharmacology, ISSN 0026-895X, 04/2017, Volume 91, Issue 4, pp. 307 - 316
Ubiquitination is a versatile post-translational modification involved in nuclear factor-kappa B (NF-kappa B) activation of Toll-like receptor (TLR) signaling.... 
REGULATOR | SIGNALING PATHWAYS | RECOGNITION | UBIQUITIN | DOWN-REGULATION | DEGRADATION | PHARMACOLOGY & PHARMACY | CELL-GROWTH | AUTOPHAGY | PROTEINS | FAMILY | Polyubiquitin - metabolism | Chemokines - biosynthesis | Toll-Like Receptor 2 - agonists | Oligonucleotide Array Sequence Analysis | Humans | Mice, Inbred C57BL | Ubiquitin-Protein Ligases - metabolism | Male | NF-kappa B - metabolism | Up-Regulation - genetics | Toll-Like Receptor 2 - metabolism | Macrophage Activation | DNA-Binding Proteins - metabolism | Ubiquitination | Animals | HEK293 Cells | TNF Receptor-Associated Factor 6 - metabolism | Protein Binding | RAW 264.7 Cells | Lysine - metabolism | Mice | Tripartite Motif Proteins - metabolism | Index Medicus
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4. Full Text Mechanism of endosomal TLR inhibition by antimalarial drugs and imidazoquinolines
by Kužnik, Alenka and Benčina, Mojca and Švajger, Urban and Jeras, Matjaž and Rozman, Blaž and Jerala, Roman
Journal of Immunology, ISSN 0022-1767, 04/2011, Volume 186, Issue 8, pp. 4794 - 4804
Endosomal TLRs play an important role in innate immune response as well as in autoimmune processes. In the therapy of systemic lupus erythematosus,... 
IMMUNOSTIMULATORY CPG-OLIGODEOXYNUCLEOTIDES | CELLS | SYSTEMIC-LUPUS-ERYTHEMATOSUS | ACTIVATION | DNA | COMPLEXES | TOLL-LIKE RECEPTORS | H+-ATPASE | IFN-ALPHA INDUCER | IMMUNOLOGY | NUCLEIC-ACIDS | Humans | Toll-Like Receptor 9 - genetics | Toll-Like Receptor 3 - antagonists & inhibitors | Endosomes - metabolism | Quinolines - pharmacology | Chloroquine - pharmacology | Quinacrine - pharmacology | Transfection | Hydrogen-Ion Concentration - drug effects | HEK293 Cells | Toll-Like Receptors - antagonists & inhibitors | Toll-Like Receptor 3 - genetics | Culture Media - chemistry | Imidazoles - metabolism | Toll-Like Receptor 8 - agonists | Binding, Competitive | Toll-Like Receptor 7 - agonists | Toll-Like Receptor 7 - genetics | Cell Line | Antimalarials - metabolism | Toll-Like Receptor 7 - metabolism | Toll-Like Receptor 9 - antagonists & inhibitors | Cytokines - metabolism | Cells, Cultured | Imidazoles - pharmacology | Nucleic Acids - metabolism | Toll-Like Receptor 3 - metabolism | Toll-Like Receptors - agonists | Antimalarials - pharmacology | Quinolines - metabolism | Animals | Toll-Like Receptors - genetics | Culture Media - pharmacology | Toll-Like Receptor 8 - genetics | Endosomes - chemistry | Toll-Like Receptor 9 - metabolism | Toll-Like Receptor 8 - metabolism | Serum - chemistry | Index Medicus | Abridged Index Medicus
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5. Full Text IgE Inhibits Toll‐like Receptor 7– and Toll‐like Receptor 9–Mediated Expression of Interferon‐α by Plasmacytoid Dendritic Cells in Patients With Systemic Lupus Erythematosus
by Khoryati, Liliane and Augusto, Jean‐François and Shipley, Emilie and Contin‐Bordes, Cécile and Douchet, Isabelle and Mitrovic, Stéphane and Truchetet, Marie‐Elise and Lazaro, Estibaliz and Duffau, Pierre and Couzi, Lionel and Jacquemin, Clément and Barnetche, Thomas and Vacher, Pierre and Schaeverbeke, Thierry and Blanco, Patrick and Richez, Christophe and Federation Hosp-Univ ACRONIM and Fédération Hospitalo-Universitaire ACRONIM
Arthritis & Rheumatology, ISSN 2326-5191, 09/2016, Volume 68, Issue 9, pp. 2221 - 2231
Objective. Plasmacytoid dendritic cells (PDCs) play a central role in pathogenesis of systemic lupus erythematosus (SLE) through their unique ability to... 
PATHOGENESIS | RESPONSES | ACTIVATION | FC-EPSILON-RI | BASOPHILS | SERUM IGE | DIFFERENTIATION | INDUCTION | RHEUMATOLOGY | AUTOIMMUNE-DISEASE | IFN-ALPHA | Toll-Like Receptor 9 - immunology | Interferon-alpha - biosynthesis | Humans | Toll-Like Receptor 7 - immunology | Cells, Cultured | Lupus Erythematosus, Systemic - immunology | Dendritic Cells - physiology | Immunoglobulin E - physiology | Index Medicus | Abridged Index Medicus
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6. Full Text Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3—mediated pathway
by Sudan He and Yuqiong Liang and Feng Shao and Xiaodong Wang
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2011, Volume 108, Issue 50, pp. 20054 - 20059
We report here that mouse macrophages undergo receptor-interacting kinase-3 (RIP3)-dependent but TNF-α—independent necrosis when Toll-like receptors (TLR) 3... 
Reactive oxygen species | Receptors | Cytokines | Cell death | Toll like receptors | Mice | Macrophages | Viability | Necrosis | Apoptosis | Necroptosis | Bone marrow-derived macrophage | INDUCED CELL-DEATH | APOPTOSIS | DOMAIN | PROTEIN | RECOGNITION | MULTIDISCIPLINARY SCIENCES | INHIBITION | LIPOPOLYSACCHARIDE | MICE | TNF-ALPHA | bone marrow-derived macrophage | NF-KAPPA-B | necroptosis | Protein Structure, Tertiary | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Reactive Oxygen Species - metabolism | Macrophages - pathology | Receptor-Interacting Protein Serine-Threonine Kinases - chemistry | NF-kappa B - metabolism | Enzyme Activation - drug effects | Toll-Like Receptor 3 - metabolism | Adaptor Proteins, Vesicular Transport - metabolism | Toll-Like Receptor 4 - metabolism | Mice, Knockout | Signal Transduction - immunology | Models, Immunological | Animals | Signal Transduction - drug effects | Protein Binding - drug effects | Inflammation Mediators - metabolism | Lipopolysaccharides - pharmacology | Interferon Regulatory Factor-3 - metabolism | Macrophages - drug effects | Cytokines - biosynthesis | Macrophages - immunology | Cell receptors | Genetic aspects | Properties | Gangrene | Signal transduction | TNF inhibitors | Kinases | Rodents | Index Medicus | Tumor necrosis factor receptors | Immune response | Data processing | Inflammation | Interleukin 1 receptors | TLR4 protein | adaptor proteins | TLR3 protein | Lipopolysaccharides | Infection | beta -Interferon | Toll-like receptors | Biological Sciences
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7. Full Text Cross‐talk between toll‐like receptor 4 (TLR4) and proteinase‐activated receptor 2 (PAR2) is involved in vascular function
by Bucci, M and Vellecco, V and Harrington, L and Brancaleone, V and Roviezzo, F and Mattace Raso, G and Ianaro, A and Lungarella, G and De Palma, R and Meli, R and Cirino, G
British Journal of Pharmacology, ISSN 0007-1188, 01/2013, Volume 168, Issue 2, pp. 411 - 420
BACKGROUND AND PURPOSE Proteinase-activated receptors (PARs) and toll-like receptors (TLRs) are involved in innate immune responses. The aim of this study was... 
PAR | hypotension | vasodilatation | TLR | TLR4 | RECOGNITION | CARDIOVASCULAR-SYSTEM | RATS | MAJOR ROLE | ARRIVE GUIDELINES | IN-VIVO | PHARMACOLOGY & PHARMACY | NF-KAPPA-B | C57BL/10SCCR MICE | PROTEASE | INNATE IMMUNITY | Oligopeptides | Rats, Wistar | Mice, Inbred C57BL | Rats | Male | Hypotension - chemically induced | Lipopolysaccharides | Mice, Knockout | Toll-Like Receptor 4 - physiology | Animals | Hypotension - physiopathology | Aorta, Thoracic - physiology | Receptor, PAR-2 - physiology | Mice | Vasodilation - physiology | In Vitro Techniques | Physiological aspects | Endothelin | Analysis | Resveratrol | Index Medicus | Themed Section | PAR2
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8. Full Text Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid-induced ceramide biosynthesis in mice
by Holland, William L and Bikman, Benjamin T and Wang, Li-Ping and Yuguang, Guan and Sargent, Katherine M and Bulchand, Sarada and Knotts, Trina A and Shui, Guanghou and Clegg, Deborah J and Wenk, Markus R and Pagliassotti, Michael J and Scherer, Philipp E and Summers, Scott A
Journal of Clinical Investigation, ISSN 0021-9738, 05/2011, Volume 121, Issue 5, pp. 1858 - 1870
Obesity is associated with an enhanced inflammatory response that exacerbates insulin resistance and contributes to diabetes, atherosclerosis, and... 
3T3-L1 ADIPOCYTES | MEDICINE, RESEARCH & EXPERIMENTAL | SKELETAL-MUSCLE | SPHINGOLIPID BIOSYNTHESIS | IMMUNE-RESPONSE | TOLL-LIKE RECEPTOR-4 | INHIBITOR MYRIOCIN | ACCUMULATION | DIET-INDUCED OBESITY | NF-KAPPA-B | ADIPOSE-TISSUE | Sphingolipids - chemistry | Soybeans | Ceramides - metabolism | Cytokines - metabolism | Hyperlipidemias - metabolism | Mice, Inbred C57BL | Insulin Resistance | Rats | Toll-Like Receptor 4 - genetics | Male | Toll-Like Receptor 4 - chemistry | I-kappa B Proteins - metabolism | Rats, Sprague-Dawley | Obesity - metabolism | Inflammation - metabolism | Lipids - chemistry | Animals | Glucose - metabolism | Mice | Mice, Inbred BALB C | Diabetes Mellitus, Experimental - metabolism | Fatty Acids - metabolism | Toll-like receptors | Physiological aspects | Ceramides | Insulin resistance | Lipids | Research | Risk factors | Index Medicus | Abridged Index Medicus
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9. Full Text SIGIRR, a negative regulator of Toll-like receptor-interleukin 1 receptor signaling
by Qian, Youcun and Towne, Jennifer and Sims, John E and Li, Xiaoxia and Wald, David and Tian, Liping and Qin, Jinzhong and Naramura, Mayumi and Zhao, Zhendong and Stark, George R
Nature Immunology, ISSN 1529-2908, 09/2003, Volume 4, Issue 9, pp. 920 - 927
The Toll-like receptor-interleukin 1 receptor signaling (TLR-IL-1R) receptor superfamily is important in differentially recognizing pathogen products and... 
IRAK | ACTIVATION | RECOGNITION | MEMBRANE | KINASE | LIPOPOLYSACCHARIDE | INTERLEUKIN-1 RECEPTOR | IMMUNOLOGY | NF-KAPPA-B | MYD88 | CUTTING EDGE | Interleukin-18 - immunology | Humans | NF-kappa B - immunology | Transcription Factor AP-1 - immunology | Immunoblotting | Receptors, Cell Surface - antagonists & inhibitors | Lipopolysaccharides - immunology | RNA - genetics | Signal Transduction - immunology | Toll-Like Receptors | Membrane Glycoproteins - antagonists & inhibitors | Interleukin-1 - immunology | Membrane Glycoproteins - immunology | Chemokines - immunology | Jurkat Cells | Receptors, Interleukin-1 - immunology | Mice, Inbred C57BL | Gene Expression Regulation | RNA - chemistry | Receptors, Cell Surface - immunology | Mice, Knockout | Animals | Chemokines - metabolism | Mice | Mice, Inbred BALB C | Index Medicus
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10. Full Text Regulation of peroxisome proliferator‐activated receptor β/δ expression and activity levels by toll‐like receptor agonists and MAP kinase inhibitors in rat astrocytes
by Chistyakov, Dmitry V and Aleshin, Stepan and Sergeeva, Marina G and Reiser, Georg
Journal of Neurochemistry, ISSN 0022-3042, 08/2014, Volume 130, Issue 4, pp. 563 - 574
Peroxisome proliferator‐activated receptor β/δ (PPARβ/δ) is a potential regulator of neuroinflammation. Toll‐like receptors (TLR) are innate immunity‐related... 
toll‐like receptors | superinduction | peroxisome proliferator‐activated receptors | inflammation | toll-like receptors | peroxisome proliferator-activated receptors | PPAR-ALPHA | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | DRUG DISCOVERY | DOWN-REGULATION | NEUROSCIENCES | BRAIN ASTROCYTES | CYCLOHEXIMIDE | MESSENGER-RNA | NF-KAPPA-B | INNATE IMMUNITY | Tumor Necrosis Factor-alpha - metabolism | Transcription, Genetic - drug effects | RNA - genetics | RNA, Messenger - biosynthesis | RNA - isolation & purification | Protein Processing, Post-Translational - drug effects | PPAR delta - biosynthesis | Enzyme Induction - drug effects | PPAR delta - drug effects | Real-Time Polymerase Chain Reaction | PPAR delta - genetics | Astrocytes - drug effects | Enzyme-Linked Immunosorbent Assay | RNA, Messenger - genetics | Rats | Blotting, Western | Toll-Like Receptors - agonists | Dinoprostone - metabolism | RNA - biosynthesis | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cyclooxygenase 2 - metabolism | Lipopolysaccharides - pharmacology | Protein Kinase Inhibitors - pharmacology | Primary Cell Culture | Astrocytes - metabolism | Index Medicus
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11. Full Text Kinase RIP3 Is Dispensable for Normal NF-κBs, Signaling by the B-Cell and T-Cell Receptors, Tumor Necrosis Factor Receptor 1, and Toll-Like Receptors 2 and 4
by Kim Newton and Xiaoqing Sun and Vishva M. Dixit
Molecular and Cellular Biology, ISSN 0270-7306, 02/2004, Volume 24, Issue 4, pp. 1464 - 1469
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
Protein Kinases - metabolism | Toll-Like Receptor 2 | Protein Kinases - genetics | Membrane Glycoproteins - metabolism | T-Lymphocytes - enzymology | Receptor-Interacting Protein Serine-Threonine Kinases | NF-kappa B - metabolism | Antigens, CD - metabolism | Toll-Like Receptors | T-Lymphocytes - metabolism | Gene Deletion | Cell Differentiation | B-Lymphocytes - metabolism | Receptors, Tumor Necrosis Factor - metabolism | B-Lymphocytes - cytology | B-Lymphocytes - enzymology | Signal Transduction | Receptors, Tumor Necrosis Factor, Type I | Cells, Cultured | Receptors, Cell Surface - metabolism | Macrophages - cytology | Killer Cells, Natural - enzymology | Macrophages - enzymology | Killer Cells, Natural - cytology | Macrophages - metabolism | Animals | T-Lymphocytes - cytology | Mice | Killer Cells, Natural - metabolism | Apoptosis | Index Medicus | Mammalian Genetic Models with Minimal or Complex Phenotypes
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