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The Journal of Immunology, ISSN 0022-1767, 01/2004, Volume 172, Issue 1, pp. 567 - 576
The signaling mechanism by which the anti-inflammatory cytokine IL-10 mediates suppression of proinflammatory cytokine synthesis remains largely unknown.... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | DNA-BINDING | HUMAN NEUTROPHILS | TYROSINE PHOSPHORYLATION | INTERLEUKIN-10 RECEPTOR | GENE-EXPRESSION | KAPPA-B-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | MONONUCLEAR PHAGOCYTES | Protein Binding - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Humans | Tumor Necrosis Factor-alpha - genetics | Immunoglobulins - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Repressor Proteins - antagonists & inhibitors | Antigens, CD - metabolism | Trans-Activators - physiology | Protein Tyrosine Phosphatases - antagonists & inhibitors | RNA, Messenger - biosynthesis | Protein Tyrosine Phosphatases - genetics | Inflammation Mediators - physiology | Glycoproteins - genetics | DNA-Binding Proteins - physiology | Protein Tyrosine Phosphatases - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Signal Transduction - genetics | DNA - metabolism | Down-Regulation - genetics | Macrophages - metabolism | Protein Tyrosine Phosphatase, Non-Receptor Type 2 | Repressor Proteins - biosynthesis | Up-Regulation - immunology | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Adenoviruses, Human - genetics | Interleukin-10 - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phosphorylation | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Antigens, CD - biosynthesis | Receptors, Cell Surface | Receptors, IgG - biosynthesis | Receptors, IgG - antagonists & inhibitors | Interleukin-10 - physiology | Signal Transduction - immunology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Signaling Lymphocytic Activation Molecule Family Member 1 | Receptors, Tumor Necrosis Factor - antagonists & inhibitors | RNA, Messenger - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type II | Trans-Activators - genetics | Inflammation Mediators - antagonists & inhibitors | Trans-Activators - biosynthesis | Immunoglobulins - biosynthesis | Macrophages - immunology | Inflammation Mediators - immunology | Receptors, Tumor Necrosis Factor - metabolism | Immune Sera - pharmacology | Proteins - physiology | Cells, Cultured | Glycoproteins - antagonists & inhibitors | Histocompatibility Antigens Class II - biosynthesis | Tissue Inhibitor of Metalloproteinase-1 - antagonists & inhibitors | Transcription Factors - antagonists & inhibitors | Transcription Factors - biosynthesis | Up-Regulation - genetics | DNA-Binding Proteins - genetics | DNA - antagonists & inhibitors | Glycoproteins - biosynthesis | Suppressor of Cytokine Signaling 3 Protein | Down-Regulation - immunology | Interleukin-6 - biosynthesis | Receptors, Tumor Necrosis Factor - biosynthesis | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Genetic Vectors | DNA-Binding Proteins - biosynthesis | Tumor Necrosis Factor-alpha - antagonists & inhibitors | SOCS-3 protein | Index Medicus | Abridged Index Medicus
Journal Article
Immunobiology, ISSN 0171-2985, 2013, Volume 218, Issue 12, pp. 1439 - 1451
Abstract Background Although the etiology of two major forms of inflammatory bowel disease (IBD), Crohn's disease (CD) and ulcerative colitis (UC) are unknown... 
Allergy and Immunology | Advanced Basic Science | Pegylated | Inflammatory bowel disease (IBD) | Leptin | Inflammation | Crohn's disease (CD) | Antagonist | Ulcerative colitis (UC) | IMMUNE-RESPONSE | TGF-BETA | CROHNS-DISEASE | ULCERATIVE-COLITIS | IMMUNOLOGY | AUTOIMMUNE ENCEPHALOMYELITIS | CUTTING EDGE | INTESTINAL INFLAMMATION | STAT3 ACTIVATION | INFLAMMATORY-BOWEL-DISEASE | REGULATORY T-CELLS | Body Weight - drug effects | Polyethylene Glycols - chemistry | Intestinal Mucosa - drug effects | Antigens, CD - metabolism | T-Lymphocytes, Regulatory - immunology | STAT1 Transcription Factor - metabolism | Intestinal Mucosa - immunology | Leptin - analogs & derivatives | Female | Leptin - administration & dosage | Colitis - drug therapy | Colitis - immunology | Smad7 Protein - genetics | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Smad7 Protein - metabolism | Leptin - chemistry | Mice, Inbred C57BL | Apyrase - metabolism | Recombinant Proteins - chemistry | Down-Regulation - drug effects | STAT1 Transcription Factor - genetics | Recombinant Proteins - administration & dosage | Mice, Knockout | Insulin - metabolism | T-Lymphocytes, Regulatory - drug effects | Animals | Signal Transduction - drug effects | Interleukin-10 - genetics | Mice | Chronic Disease | Transforming Growth Factor beta - metabolism | Index Medicus | Crohn’s Disease (CD) | Ulcerative Colitis (UC)
Journal Article
The Journal of Immunology, ISSN 0022-1767, 06/2002, Volume 168, Issue 12, pp. 6404 - 6411
Previous studies have shown that IL-10 can induce the expression of the suppressor of cytokine signaling 3 (SOCS-3) mRNA in human monocytes and neutrophils,... 
EXPERIMENTAL ENDOTOXEMIA | TUMOR-NECROSIS-FACTOR | CHRONIC ENTEROCOLITIS | HUMAN NEUTROPHILS | MESSENGER-RNA | INTERFERON-GAMMA | NEGATIVE REGULATION | INTERLEUKIN-10 RECEPTOR | TNF-ALPHA | IMMUNOLOGY | HUMAN MONOCYTES | Sialoglycoproteins - genetics | Protein Biosynthesis | Interleukin-6 - antagonists & inhibitors | Repressor Proteins | Tumor Necrosis Factor-alpha - genetics | Lipopolysaccharides - antagonists & inhibitors | RNA, Messenger - metabolism | Suppressor of Cytokine Signaling Proteins | Nitric Oxide Synthase Type II | RNA, Messenger - biosynthesis | Sialoglycoproteins - biosynthesis | Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis | Interleukin-6 - metabolism | Nitric Oxide - biosynthesis | DNA-Binding Proteins - antagonists & inhibitors | Interleukin-6 - genetics | Macrophage Activation - immunology | Macrophages, Peritoneal - immunology | Signal Transduction - genetics | Mice, Knockout | Macrophages - metabolism | Up-Regulation - immunology | Lipopolysaccharides - pharmacology | Mice | Transcription Factors | Macrophages, Peritoneal - metabolism | Tumor Necrosis Factor-alpha - biosynthesis | Macrophage Activation - genetics | Nitric Oxide Synthase - antagonists & inhibitors | Nitric Oxide Synthase - genetics | MAP Kinase Signaling System - immunology | Interleukin-10 - physiology | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Transfection | RNA, Messenger - antagonists & inhibitors | Nitric Oxide Synthase - biosynthesis | Macrophages - immunology | Cell Line | Proteins - physiology | Nitric Oxide - antagonists & inhibitors | Mice, Inbred C57BL | Cells, Cultured | Up-Regulation - genetics | Proteins - genetics | Suppressor of Cytokine Signaling 3 Protein | Animals | Granulocyte-Macrophage Colony-Stimulating Factor - antagonists & inhibitors | Interleukin 1 Receptor Antagonist Protein | Trans-Activators - metabolism | STAT3 Transcription Factor | Trans-Activators - antagonists & inhibitors | Receptors, Interleukin-1 - antagonists & inhibitors | Interleukin-10 - pharmacology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Index Medicus | Abridged Index Medicus
Journal Article
Molecular Nutrition & Food Research, ISSN 1613-4125, 08/2015, Volume 59, Issue 8, pp. 1524 - 1534
Inflammatory response of macrophages is regulated by vitamin E forms. The long-chain metabolite α-13'-carboxychromanol (α-13'-COOH) is formed by hepatic... 
Macrophage activation | α‐13’‐COOH | Inflammation | Inflammatory response | α‐Tocopherol | Macrophages | Inflammatoryresponse | α-13'-COOH | α-Tocopherol | Prostaglandin D2 - antagonists & inhibitors | Immunomodulation - drug effects | alpha-Tocopherol - analogs & derivatives | Benzopyrans - metabolism | Interleukin-1beta - genetics | Lipopolysaccharides - antagonists & inhibitors | Dinoprost - metabolism | Cyclooxygenase 2 - genetics | Interleukin-1beta - metabolism | Nitric Oxide Synthase Type II - antagonists & inhibitors | Prostaglandin D2 - metabolism | Interleukin-10 - metabolism | Anti-Inflammatory Agents, Non-Steroidal - metabolism | alpha-Tocopherol - metabolism | Fatty Acids - metabolism | Macrophages - immunology | Interleukin-1beta - antagonists & inhibitors | Nitric Oxide - antagonists & inhibitors | Cyclooxygenase 2 - chemistry | Dinoprostone - metabolism | Gene Expression Regulation - drug effects | Macrophages - metabolism | Animals | Nitric Oxide Synthase Type II - genetics | Transcription Factor RelA - metabolism | Active Transport, Cell Nucleus - drug effects | Interleukin-10 - antagonists & inhibitors | Interleukin-10 - genetics | Cyclooxygenase 2 - metabolism | Lipopolysaccharides - pharmacology | Dinoprost - antagonists & inhibitors | Macrophages - drug effects | RAW 264.7 Cells | Mice | Dinoprostone - antagonists & inhibitors | Macrophage Activation - drug effects | Nitric Oxide - metabolism | Nitric Oxide Synthase Type II - metabolism | Index Medicus
Journal Article
Journal Article
Journal Article
The Journal of Immunology, ISSN 0022-1767, 03/2003, Volume 170, Issue 6, pp. 3263 - 3272
On human macrophages IL-10 acts as a more potent anti-inflammatory cytokine than IL-6, although both cytokines signal mainly via activation of the... 
Tumor Necrosis Factor-alpha - metabolism | Protein Biosynthesis | Protein Tyrosine Phosphatase, Non-Receptor Type 11 | Interleukin-6 - antagonists & inhibitors | Tetradecanoylphorbol Acetate - pharmacology | Humans | Repressor Proteins | Protein Tyrosine Phosphatases - metabolism | Lipopolysaccharides - antagonists & inhibitors | Suppressor of Cytokine Signaling Proteins | MAP Kinase Signaling System - immunology | Enzyme Activation - immunology | Interleukin-10 - physiology | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Trans-Activators - physiology | DNA-Binding Proteins - metabolism | Signal Transduction - immunology | Anti-Inflammatory Agents, Non-Steroidal - antagonists & inhibitors | Feedback, Physiological - immunology | Inflammation Mediators - pharmacology | Interleukin-6 - physiology | Inflammation Mediators - antagonists & inhibitors | Macrophages - immunology | Proteins - physiology | DNA-Binding Proteins - physiology | DNA-Binding Proteins - antagonists & inhibitors | Cells, Cultured | Enzyme Inhibitors - pharmacology | Intracellular Signaling Peptides and Proteins | Macrophages - enzymology | Suppressor of Cytokine Signaling 3 Protein | Macrophages - metabolism | Signal Transduction - drug effects | Interleukin-10 - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Trans-Activators - metabolism | STAT3 Transcription Factor | Transcription Factors | Trans-Activators - antagonists & inhibitors | Interleukin-10 - pharmacology | Mitogen-Activated Protein Kinase 3 | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
European Spine Journal, ISSN 0940-6719, 3/2012, Volume 21, Issue 3, pp. 537 - 545
The symptoms of lumbar disc herniation, such as low back pain and sciatica, have been associated with local release of cytokines following the inflammatory... 
Surgical Orthopedics | Medicine & Public Health | Lumbar disc herniation | Radicular pain | Neurosurgery | Dorsal root ganglion | Hyperalgesia | LUMBAR INTERVERTEBRAL DISCS | WALLERIAN DEGENERATION | RATS | NECROSIS-FACTOR-ALPHA | DORSAL-ROOT GANGLION | CLINICAL NEUROLOGY | EXPERIMENTAL DISC HERNIATION | SPINAL NERVE ROOTS | PAIN | FUNCTIONAL-CHANGES | NITRIC-OXIDE | ORTHOPEDICS | Interleukin-1beta - physiology | Interleukin-6 - antagonists & inhibitors | Rats, Wistar | Chemokine CXCL1 - antagonists & inhibitors | Hyperalgesia - prevention & control | Rats | Male | Antibodies - physiology | Cytokines - physiology | Interleukin-10 - physiology | Hyperalgesia - pathology | Hyperalgesia - immunology | Animals | Time Factors | Chemokine CXCL1 - physiology | Interleukin-10 - antagonists & inhibitors | Interleukin-6 - physiology | Tumor Necrosis Factor-alpha - physiology | Inflammation Mediators - antagonists & inhibitors | Cytokines - antagonists & inhibitors | Intervertebral Disc - pathology | Inflammation Mediators - physiology | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Interleukin-1beta - antagonists & inhibitors | Viral antibodies | Cytokines | Animal behavior | Analysis | Antibodies | Inflammation | Backache | Chronic pain | Index Medicus | Spinal nerves | Animal models | Pain perception | Low back pain | Spine (lumbar) | Mechanical properties | Intervertebral discs | Dorsal root ganglia | nucleus pulposus | Interleukin 1 | Tumor necrosis factor- alpha | Original
Journal Article
American Journal of Respiratory Cell and Molecular Biology, ISSN 1044-1549, 10/2013, Volume 49, Issue 4, pp. 552 - 562
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are characterized by pulmonary edema attributable to alveolar... 
Alveolar injury | Inflammation | Cell therapy | IL-33 | BIOCHEMISTRY & MOLECULAR BIOLOGY | MECHANISMS | SEPSIS | MODEL | TRANSPLANTATION | CELL BIOLOGY | RESPONSES | alveolar injury | ENGRAFTMENT | INHIBITION | inflammation | RESPIRATORY SYSTEM | cell therapy | HOST-DEFENSE | LIPOPOLYSACCHARIDE | GENE-THERAPY | Bronchoalveolar Lavage Fluid | Inflammation - chemically induced | Tumor Necrosis Factor-alpha - metabolism | Humans | Tumor Necrosis Factor-alpha - genetics | Endotoxins | Acute Lung Injury - genetics | Male | Interferon-gamma - metabolism | Interleukin-1beta - genetics | Interleukins - metabolism | Receptors, Somatostatin - genetics | Interleukins - genetics | Inflammation - metabolism | Mesenchymal Stromal Cells - cytology | Interleukin-1beta - metabolism | HEK293 Cells | Interleukin-10 - metabolism | Female | Acute Lung Injury - metabolism | Interferon-gamma - genetics | Acute Lung Injury - surgery | Mesenchymal Stromal Cells - physiology | Interleukin-33 | Mesenchymal Stromal Cells - metabolism | Toll-Like Receptor 4 - chemistry | Toll-Like Receptor 4 - metabolism | Interleukins - antagonists & inhibitors | Mesenchymal Stem Cell Transplantation - methods | Receptors, Somatostatin - biosynthesis | Animals | Interleukin-10 - genetics | Lipopolysaccharides - pharmacology | Inflammation - genetics | Mice | Mice, Inbred BALB C | Index Medicus
Journal Article
European Journal of Immunology, ISSN 0014-2980, 02/2011, Volume 41, Issue 2, pp. 413 - 424
During infection, TLR agonists are released and trigger mature as well as differentiating innate immune cells. Early encounter with TLR agonists (R848; LPS)... 
PD-L1 | Tolerance | STAT-3 | TLR | DC | MYCOBACTERIUM-TUBERCULOSIS | ALLOGRAFT-REJECTION | HUMAN DENDRITIC CELLS | IFN-GAMMA | TRANSPLANT TOLERANCE | IMMUNOLOGY | CUTTING EDGE | IMMUNE-RESPONSES | REGULATORY T-CELLS | B7 FAMILY | DIFFERENTIATION | T-Lymphocyte Subsets - immunology | Antigen-Presenting Cells - cytology | Immune Tolerance - physiology | Monocytes - cytology | Dendritic Cells - immunology | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | STAT Transcription Factors - metabolism | Monocytes - immunology | Antigens, CD - metabolism | Lipopolysaccharide Receptors - metabolism | Lymphocyte Culture Test, Mixed | T-Lymphocytes, Regulatory - immunology | Signal Transduction - immunology | Interleukin-4 - pharmacology | Interleukin-10 - metabolism | Histocompatibility Antigens Class II - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Interleukin-6 - metabolism | STAT3 Transcription Factor - metabolism | Antigen-Presenting Cells - metabolism | B7-H1 Antigen | Gene Expression Regulation - immunology | Antigen-Presenting Cells - drug effects | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology | Imidazoles - pharmacology | Antigen-Presenting Cells - immunology | Toll-Like Receptors - agonists | Monocytes - drug effects | Cell Differentiation - immunology | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Differentiation - drug effects | Antigens, CD1 - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Dendritic Cells - cytology | Protein Kinase Inhibitors - pharmacology | STAT Transcription Factors - antagonists & inhibitors | STAT3 Transcription Factor - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism | Medical research | Rodents | Index Medicus
Journal Article
Cell Communication and Signaling, ISSN 1478-811X, 2014, Volume 12, Issue 1, pp. 1 - 13
Background: B cells are important effectors and regulators of adaptive and innate immune responses, inflammation and autoimmunity, for instance in... 
B cell | B10 | Ifenprodil | Memantine | K Ca 3.1 | 3.1 | 1.3 | Nmda-receptor antagonist | K v 1.3 | IL-10 | LPS | NMDA-receptor antagonist | K(v)1.3 | ACTIVATION | POTASSIUM CHANNELS | ALZHEIMERS-DISEASE | B10 CELLS | AUTOIMMUNE ENCEPHALOMYELITIS | CELL BIOLOGY | K(Ca)3.1 | TOLL-LIKE RECEPTORS | ION CHANNELS | LYMPHOCYTE FUNCTION | EXPRESSION | T-CELLS | Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors | Apoptosis - drug effects | Mice, Inbred C57BL | Mice, Transgenic | Interferon-gamma - metabolism | Receptors, Antigen, B-Cell - metabolism | Intermediate-Conductance Calcium-Activated Potassium Channels - metabolism | Toll-Like Receptor 4 - metabolism | Immunoglobulin M - metabolism | B-Lymphocytes - drug effects | Animals | CD40 Antigens - metabolism | Piperidines - pharmacology | Interleukin-10 - genetics | Lipopolysaccharides - pharmacology | Interleukin-10 - metabolism | Kv1.3 Potassium Channel - metabolism | Cell Proliferation - drug effects | B-Lymphocytes - metabolism | Immunoglobulin G - metabolism | Autoimmunity | Encephalitis | Methyl aspartate | Care and treatment | Immunoglobulin G | B cells | Diagnosis | Health aspects | Alzheimer's disease | Risk factors | Immune response | Mitogens | Competition | Antigens | Neurosciences | Multiple sclerosis | Statistical analysis | Experiments | Cell adhesion & migration | Cell growth | Rodents | Ligands | Alzheimers disease | Binding sites | Immune system | Apoptosis | Index Medicus
Journal Article
The Journal of Immunology, ISSN 0022-1767, 12/2004, Volume 173, Issue 12, pp. 7548 - 7555
Recognition of microbial products through TLRs triggers the expression of several cytokines that regulate innate and adaptive immunity. Signaling by various... 
TOLL-LIKE RECEPTOR-2 | RESPONSES | IN-VITRO | INTERFERON-GAMMA | SIGNALING PATHWAY | MACROPHAGES | GENE-EXPRESSION | MICE | IMMUNOLOGY | T-CELLS | CUTTING EDGE | Cysteine - analogs & derivatives | Leukocytes, Mononuclear - metabolism | Toll-Like Receptor 2 | Toll-Like Receptor 3 | Toll-Like Receptor 4 | Dendritic Cells - immunology | Humans | Receptors, Cell Surface - antagonists & inhibitors | Th1 Cells - immunology | Toll-Like Receptor 5 | Interleukin-10 - physiology | Toll-Like Receptor 7 | Th1 Cells - metabolism | Toll-Like Receptors | Membrane Glycoproteins - antagonists & inhibitors | Autocrine Communication - immunology | Protein Isoforms - agonists | Interleukin-12 - antagonists & inhibitors | Leukocytes, Mononuclear - immunology | Cysteine - pharmacology | Interleukin-10 - metabolism | Chemokines, CXC - biosynthesis | Cytokines - genetics | Dendritic Cells - metabolism | Interleukin-12 - biosynthesis | Chemokines, CXC - antagonists & inhibitors | Poly I-C - pharmacology | Membrane Glycoproteins - pharmacology | Membrane Glycoproteins - agonists | Receptors, Cell Surface - agonists | Down-Regulation - genetics | Autocrine Communication - genetics | Chemokine CXCL10 | Protein Isoforms - pharmacology | Down-Regulation - immunology | Lipoproteins - pharmacology | Lipopolysaccharides - pharmacology | Cytokines - antagonists & inhibitors | Peptidoglycan - pharmacology | Cytokines - biosynthesis | Drug Combinations | Protein Isoforms - antagonists & inhibitors | Index Medicus | Abridged Index Medicus
Journal Article