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Publication DateCellular Microbiology, ISSN 1462-5814, 06/2006, Volume 8, Issue 6, pp. 1047 - 1057
Summary Infection of epithelial cells by the intracellular pathogen, Chlamydia trachomatis, leads to activation of NF-κB and secretion of pro-inflammatory...
GENITAL-TRACT INFECTION | DEVELOPMENTAL CYCLE | MOUSE PNEUMONITIS | IFN-GAMMA | TOLL-LIKE RECEPTORS | INNATE IMMUNE-RESPONSE | MICROBIOLOGY | EPITHELIAL-CELL LINES | BACTERIAL PEPTIDOGLYCAN | INFLAMMATORY RESPONSE | NF-KAPPA-B | CELL BIOLOGY | Toll-Like Receptor 2 - genetics | Fibroblasts - physiology | Receptor-Interacting Protein Serine-Threonine Kinases | Chlamydia trachomatis - chemistry | Humans | Receptors, Cell Surface - analysis | Epithelium - chemistry | RNA, Messenger - analysis | Male | Chlamydia Infections - pathology | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins - physiology | Epithelium - microbiology | Chlamydia Infections - physiopathology | DNA, Bacterial - analysis | Female | Chlamydia muridarum - physiology | Receptor-Interacting Protein Serine-Threonine Kinase 2 | Receptors, Cell Surface - physiology | Fibroblasts - microbiology | NF-kappa B - analysis | Epithelium - pathology | Protein-Serine-Threonine Kinases - physiology | RNA, Messenger - genetics | Toll-Like Receptor 4 - genetics | Chlamydia muridarum - chemistry | Gene Expression Regulation, Bacterial - physiology | Toll-Like Receptor 4 - physiology | Adaptor Proteins, Signal Transducing - physiology | Animals | DNA, Bacterial - genetics | Toll-Like Receptor 2 - physiology | Chlamydia muridarum - pathogenicity | Adaptor Proteins, Signal Transducing - genetics | Chlamydia trachomatis - pathogenicity | NF-kappa B - physiology | Mice, Inbred NOD | Epithelium - physiology | Mice | Nod1 Signaling Adaptor Protein | Vagina - microbiology | HeLa Cells | Chlamydia trachomatis - physiology | Chlamydia | Health aspects | Sexually transmitted diseases | Toll-Like Receptor 2 | Toll-Like Receptor 4 | Protein-Serine-Threonine Kinases | Receptors, Cell Surface | Innate immunity | Chlamydia trachomatis | DNA, Bacterial | Life Sciences | NF-kappa B | Immunology | Chlamydia Infections | Fibroblasts | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins | Vagina | Epithelium | Adaptor Proteins, Signal Transducing | Gene Expression Regulation, Bacterial | RNA, Messenger | Hela Cells | Chlamydia muridarum
GENITAL-TRACT INFECTION | DEVELOPMENTAL CYCLE | MOUSE PNEUMONITIS | IFN-GAMMA | TOLL-LIKE RECEPTORS | INNATE IMMUNE-RESPONSE | MICROBIOLOGY | EPITHELIAL-CELL LINES | BACTERIAL PEPTIDOGLYCAN | INFLAMMATORY RESPONSE | NF-KAPPA-B | CELL BIOLOGY | Toll-Like Receptor 2 - genetics | Fibroblasts - physiology | Receptor-Interacting Protein Serine-Threonine Kinases | Chlamydia trachomatis - chemistry | Humans | Receptors, Cell Surface - analysis | Epithelium - chemistry | RNA, Messenger - analysis | Male | Chlamydia Infections - pathology | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins - physiology | Epithelium - microbiology | Chlamydia Infections - physiopathology | DNA, Bacterial - analysis | Female | Chlamydia muridarum - physiology | Receptor-Interacting Protein Serine-Threonine Kinase 2 | Receptors, Cell Surface - physiology | Fibroblasts - microbiology | NF-kappa B - analysis | Epithelium - pathology | Protein-Serine-Threonine Kinases - physiology | RNA, Messenger - genetics | Toll-Like Receptor 4 - genetics | Chlamydia muridarum - chemistry | Gene Expression Regulation, Bacterial - physiology | Toll-Like Receptor 4 - physiology | Adaptor Proteins, Signal Transducing - physiology | Animals | DNA, Bacterial - genetics | Toll-Like Receptor 2 - physiology | Chlamydia muridarum - pathogenicity | Adaptor Proteins, Signal Transducing - genetics | Chlamydia trachomatis - pathogenicity | NF-kappa B - physiology | Mice, Inbred NOD | Epithelium - physiology | Mice | Nod1 Signaling Adaptor Protein | Vagina - microbiology | HeLa Cells | Chlamydia trachomatis - physiology | Chlamydia | Health aspects | Sexually transmitted diseases | Toll-Like Receptor 2 | Toll-Like Receptor 4 | Protein-Serine-Threonine Kinases | Receptors, Cell Surface | Innate immunity | Chlamydia trachomatis | DNA, Bacterial | Life Sciences | NF-kappa B | Immunology | Chlamydia Infections | Fibroblasts | Tumor Necrosis Factor Receptor-Associated Peptides and Proteins | Vagina | Epithelium | Adaptor Proteins, Signal Transducing | Gene Expression Regulation, Bacterial | RNA, Messenger | Hela Cells | Chlamydia muridarum
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Loading RightsImmunology, ISSN 0019-2805, 11/2013, Volume 140, Issue 3, pp. 352 - 361
Summary The effect of Pam3CSK4, a Toll‐like receptor 2 (TLR2) ligand, on interferon‐γ (IFN‐γ) ‐induced nitric oxide (NO) production in mouse vascular...
interferon‐γ receptor | Pam3CSK4 | vascular endothelial cells | MyD88 | Toll‐like receptor 2 | Vascular endothelial cells | Interferon-γ receptor | Toll-like receptor 2 | ACTIVATION | interferon- receptor | IFN-GAMMA | MACROPHAGES | CPG-DNA | STAT1 PHOSPHORYLATION | NECROSIS-FACTOR-ALPHA | SIGNAL INTEGRATION | IMMUNOLOGY | SERINE PHOSPHORYLATION | LIPOPOLYSACCHARIDE | INNATE IMMUNITY | Cell Line | Toll-Like Receptor 2 - agonists | Lipopeptides - pharmacology | Endothelium, Vascular - drug effects | Receptors, Interferon - metabolism | Gene Expression Regulation - drug effects | Animals | MAP Kinase Kinase 4 - metabolism | MAP Kinase Signaling System - drug effects | Nitric Oxide Synthase Type II - genetics | Interferon-Stimulated Gene Factor 3 - metabolism | Interferon-gamma - immunology | Protein Binding | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Nitric Oxide - metabolism | Myeloid Differentiation Factor 88 - metabolism | Endothelium, Vascular - immunology | Nitric Oxide Synthase Type II - metabolism | interferon-γ receptor | Original
interferon‐γ receptor | Pam3CSK4 | vascular endothelial cells | MyD88 | Toll‐like receptor 2 | Vascular endothelial cells | Interferon-γ receptor | Toll-like receptor 2 | ACTIVATION | interferon- receptor | IFN-GAMMA | MACROPHAGES | CPG-DNA | STAT1 PHOSPHORYLATION | NECROSIS-FACTOR-ALPHA | SIGNAL INTEGRATION | IMMUNOLOGY | SERINE PHOSPHORYLATION | LIPOPOLYSACCHARIDE | INNATE IMMUNITY | Cell Line | Toll-Like Receptor 2 - agonists | Lipopeptides - pharmacology | Endothelium, Vascular - drug effects | Receptors, Interferon - metabolism | Gene Expression Regulation - drug effects | Animals | MAP Kinase Kinase 4 - metabolism | MAP Kinase Signaling System - drug effects | Nitric Oxide Synthase Type II - genetics | Interferon-Stimulated Gene Factor 3 - metabolism | Interferon-gamma - immunology | Protein Binding | Mice | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Nitric Oxide - metabolism | Myeloid Differentiation Factor 88 - metabolism | Endothelium, Vascular - immunology | Nitric Oxide Synthase Type II - metabolism | interferon-γ receptor | Original
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Loading RightsShock, ISSN 1073-2322, 07/2014, Volume 42, Issue 1, pp. 52 - 59
ABSTRACTItraconazole (ICZ) is commonly used for the treatment of fungal infections, particularly in immunocompromised patients. In addition, ICZ has been...
phagocytosis | cancer | bacteria | Fcγ receptors | innate immunity | Macrophages | SURGERY | ACTIVATION | DRUG ITRACONAZOLE | IFN-GAMMA | LOW-DENSITY-LIPOPROTEIN | CHOLESTEROL TRAFFICKING | CELL LUNG-CANCER | Fc receptors | MESSENGER-RNA | ENDOTHELIAL-CELLS | DISEASE | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | CRITICAL CARE MEDICINE | Antifungal Agents - pharmacology | Phagocytosis - drug effects | Gene Expression Regulation - immunology | Cells, Cultured | Escherichia coli - immunology | Itraconazole - antagonists & inhibitors | Male | Glycosylation - drug effects | Mice, Inbred Strains | Receptors, IgG - antagonists & inhibitors | Itraconazole - pharmacology | Receptors, IgG - metabolism | Dose-Response Relationship, Drug | Gene Expression Regulation - drug effects | Receptors, IgG - genetics | Animals | Cholesterol, LDL - pharmacology | Itraconazole - administration & dosage | Macrophages - drug effects | Cell Membrane - metabolism | Antifungal Agents - administration & dosage | Macrophages - immunology | Fcgamma receptors
phagocytosis | cancer | bacteria | Fcγ receptors | innate immunity | Macrophages | SURGERY | ACTIVATION | DRUG ITRACONAZOLE | IFN-GAMMA | LOW-DENSITY-LIPOPROTEIN | CHOLESTEROL TRAFFICKING | CELL LUNG-CANCER | Fc receptors | MESSENGER-RNA | ENDOTHELIAL-CELLS | DISEASE | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | CRITICAL CARE MEDICINE | Antifungal Agents - pharmacology | Phagocytosis - drug effects | Gene Expression Regulation - immunology | Cells, Cultured | Escherichia coli - immunology | Itraconazole - antagonists & inhibitors | Male | Glycosylation - drug effects | Mice, Inbred Strains | Receptors, IgG - antagonists & inhibitors | Itraconazole - pharmacology | Receptors, IgG - metabolism | Dose-Response Relationship, Drug | Gene Expression Regulation - drug effects | Receptors, IgG - genetics | Animals | Cholesterol, LDL - pharmacology | Itraconazole - administration & dosage | Macrophages - drug effects | Cell Membrane - metabolism | Antifungal Agents - administration & dosage | Macrophages - immunology | Fcgamma receptors
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T helper 1 immunity requires complement-driven NLRP3 inflammasome activity in CD4+ T cells
Science, ISSN 0036-8075, 06/2016, Volume 352, Issue 6292, pp. aad1210 - aad1210
The NLRP3 inflammasome controls interleukin-1β maturation in antigen-presenting cells, but a direct role for NLRP3 in human adaptive immune cells has not been...
INTESTINAL INFLAMMATION | ACTIVATION | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | C5L2 | DISEASE | CYTOKINE | INNATE LYMPHOID-CELLS | DIFFERENTIATION | C5A RECEPTOR CD88 | ANTAGONISTS | Receptor, Anaphylatoxin C5a - agonists | Reactive Oxygen Species - metabolism | Complement Activation | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Th1 Cells - immunology | CD4-Positive T-Lymphocytes - immunology | Mice, Mutant Strains | HEK293 Cells | Receptors, Antigen, T-Cell - agonists | Receptors, Chemokine - antagonists & inhibitors | Disease Models, Animal | Adaptive Immunity | Cryopyrin-Associated Periodic Syndromes - immunology | Autocrine Communication | Receptors, Antigen, T-Cell - metabolism | Receptors, Chemokine - metabolism | Receptors, Chemokine - agonists | Inflammation - immunology | Immunity, Innate | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Inflammasomes - immunology | Mice | Complement C5a - immunology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Interferon-gamma - biosynthesis | Membrane Cofactor Protein - immunology | Receptor, Anaphylatoxin C5a - metabolism | Antigen presentation | Cellular biology | Lymphocytes | Immune system | Immune systems | Microorganisms | Interleukin | Bacteria | Activation | Complement | Immunity | Assembly
INTESTINAL INFLAMMATION | ACTIVATION | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | C5L2 | DISEASE | CYTOKINE | INNATE LYMPHOID-CELLS | DIFFERENTIATION | C5A RECEPTOR CD88 | ANTAGONISTS | Receptor, Anaphylatoxin C5a - agonists | Reactive Oxygen Species - metabolism | Complement Activation | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Th1 Cells - immunology | CD4-Positive T-Lymphocytes - immunology | Mice, Mutant Strains | HEK293 Cells | Receptors, Antigen, T-Cell - agonists | Receptors, Chemokine - antagonists & inhibitors | Disease Models, Animal | Adaptive Immunity | Cryopyrin-Associated Periodic Syndromes - immunology | Autocrine Communication | Receptors, Antigen, T-Cell - metabolism | Receptors, Chemokine - metabolism | Receptors, Chemokine - agonists | Inflammation - immunology | Immunity, Innate | Carrier Proteins - genetics | Animals | Carrier Proteins - metabolism | Inflammasomes - immunology | Mice | Complement C5a - immunology | Receptor, Anaphylatoxin C5a - antagonists & inhibitors | Interferon-gamma - biosynthesis | Membrane Cofactor Protein - immunology | Receptor, Anaphylatoxin C5a - metabolism | Antigen presentation | Cellular biology | Lymphocytes | Immune system | Immune systems | Microorganisms | Interleukin | Bacteria | Activation | Complement | Immunity | Assembly
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Loading RightsLeukemia, ISSN 0887-6924, 11/2018, Volume 32, Issue 11, pp. 2483 - 2494
The therapeutic benefits of allogeneic hematopoietic stem cell transplantation (allo-HSCT) are derived from the graft-versus leukemia (GvL) effects of the...
PRECLINICAL CHARACTERIZATION | REGULATOR | INHIBITION | IDIOPATHIC PNEUMONIA SYNDROME | ONCOLOGY | PHOSPHORYLATION | IFN-GAMMA | GVHD | STEM-CELL TRANSPLANTATION | THROMBOPOIETIN | HEMATOLOGY | EXPRESSION | Prevention | Antigens | Interleukins | Leukemia | Stem cells | Transplantation | B cells | Biological response modifiers | T cells | Health aspects | Hematopoietic stem cells | Interferon gamma | Cell proliferation | Graft-versus-host reaction | Interleukin | Stem cell transplantation | Lymphocytes T | Kinases | Grafting | Interleukin 6 | Lymphocytes | Interleukin 6 receptors | Janus kinase 2 | Janus kinase | Cell survival | Cytokines | Immunoregulation | Therapeutic applications | Medical treatment | CD80 antigen | Pharmacology | Stat5 protein | CXCR3 protein | Chemical compounds | Disease control | Hemopoiesis | Major histocompatibility complex | Antigen-presenting cells | PD-L1 protein | Interferon | Histocompatibility
PRECLINICAL CHARACTERIZATION | REGULATOR | INHIBITION | IDIOPATHIC PNEUMONIA SYNDROME | ONCOLOGY | PHOSPHORYLATION | IFN-GAMMA | GVHD | STEM-CELL TRANSPLANTATION | THROMBOPOIETIN | HEMATOLOGY | EXPRESSION | Prevention | Antigens | Interleukins | Leukemia | Stem cells | Transplantation | B cells | Biological response modifiers | T cells | Health aspects | Hematopoietic stem cells | Interferon gamma | Cell proliferation | Graft-versus-host reaction | Interleukin | Stem cell transplantation | Lymphocytes T | Kinases | Grafting | Interleukin 6 | Lymphocytes | Interleukin 6 receptors | Janus kinase 2 | Janus kinase | Cell survival | Cytokines | Immunoregulation | Therapeutic applications | Medical treatment | CD80 antigen | Pharmacology | Stat5 protein | CXCR3 protein | Chemical compounds | Disease control | Hemopoiesis | Major histocompatibility complex | Antigen-presenting cells | PD-L1 protein | Interferon | Histocompatibility
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Loading RightsNeuropsychobiology, ISSN 0302-282X, 12/2011, Volume 65, Issue 1, pp. 12 - 19
Aims: There is evidence that psychological stress can modulate immune functions. It has been hypothesized that acute stressors can affect both immune balance...
Original Paper | Acute stress | IFN-γ | Adrenergic receptor | IFN-γ receptor | Immunomodulation | Glucocorticoid receptor | beta-Adrenergic receptor | SOCIAL STRESS | PSYCHIATRY | INDUCED ANXIETY | NEUROSCIENCES | INFLAMMATORY CYTOKINE | PSYCHOLOGY | LEUKOCYTE DISTRIBUTION | MENTAL STRESS | RESPONSES | IN-VITRO | IFN-gamma | IFN-gamma receptor | MESSENGER-RNA | PSYCHOSOCIAL STRESS | ACUTE PSYCHOLOGICAL STRESS | T-Lymphocytes, Regulatory - metabolism | Catecholamines - metabolism | Humans | Middle Aged | Male | Receptors, Adrenergic, beta-2 - immunology | Receptors, Glucocorticoid - metabolism | Th2 Cells - immunology | Receptors, Catecholamine - immunology | Th1 Cells - immunology | Receptors, Catecholamine - metabolism | Stress, Psychological - immunology | T-Lymphocytes, Regulatory - immunology | Th1 Cells - metabolism | Interleukin-10 - metabolism | Adult | Female | Receptors, Cytokine - metabolism | Receptors, Catecholamine - genetics | Cytokines - genetics | Real-Time Polymerase Chain Reaction | Receptors, Cytokine - genetics | Receptors, Interferon - genetics | Transforming Growth Factor beta - immunology | Interferon-gamma | Gene Expression | Cytokines - metabolism | Receptors, Adrenergic, beta-2 - genetics | Receptors, Interleukin-4 - metabolism | Receptors, Glucocorticoid - immunology | Receptors, Interleukin-4 - immunology | Th2 Cells - metabolism | Receptors, Adrenergic, beta-2 - metabolism | Transforming Growth Factor beta - genetics | Receptors, Interferon - immunology | Interleukin-10 - genetics | Receptors, Interleukin-4 - genetics | Receptors, Glucocorticoid - genetics | Receptors, Cytokine - immunology | Interleukin-10 - immunology | Transforming Growth Factor beta - metabolism
Original Paper | Acute stress | IFN-γ | Adrenergic receptor | IFN-γ receptor | Immunomodulation | Glucocorticoid receptor | beta-Adrenergic receptor | SOCIAL STRESS | PSYCHIATRY | INDUCED ANXIETY | NEUROSCIENCES | INFLAMMATORY CYTOKINE | PSYCHOLOGY | LEUKOCYTE DISTRIBUTION | MENTAL STRESS | RESPONSES | IN-VITRO | IFN-gamma | IFN-gamma receptor | MESSENGER-RNA | PSYCHOSOCIAL STRESS | ACUTE PSYCHOLOGICAL STRESS | T-Lymphocytes, Regulatory - metabolism | Catecholamines - metabolism | Humans | Middle Aged | Male | Receptors, Adrenergic, beta-2 - immunology | Receptors, Glucocorticoid - metabolism | Th2 Cells - immunology | Receptors, Catecholamine - immunology | Th1 Cells - immunology | Receptors, Catecholamine - metabolism | Stress, Psychological - immunology | T-Lymphocytes, Regulatory - immunology | Th1 Cells - metabolism | Interleukin-10 - metabolism | Adult | Female | Receptors, Cytokine - metabolism | Receptors, Catecholamine - genetics | Cytokines - genetics | Real-Time Polymerase Chain Reaction | Receptors, Cytokine - genetics | Receptors, Interferon - genetics | Transforming Growth Factor beta - immunology | Interferon-gamma | Gene Expression | Cytokines - metabolism | Receptors, Adrenergic, beta-2 - genetics | Receptors, Interleukin-4 - metabolism | Receptors, Glucocorticoid - immunology | Receptors, Interleukin-4 - immunology | Th2 Cells - metabolism | Receptors, Adrenergic, beta-2 - metabolism | Transforming Growth Factor beta - genetics | Receptors, Interferon - immunology | Interleukin-10 - genetics | Receptors, Interleukin-4 - genetics | Receptors, Glucocorticoid - genetics | Receptors, Cytokine - immunology | Interleukin-10 - immunology | Transforming Growth Factor beta - metabolism
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Loading RightsClinical Infectious Diseases, ISSN 1058-4838, 9/2009, Volume 49, Issue 6, pp. e62 - e65
Severe coccidioidomycosis is rare, and specific genetic susceptibility to the disease remains unidentified. We describe a patient with disseminated...
AUTOANTIBODIES | INFECTIOUS DISEASES | INFECTIONS | IFN-GAMMA | TUBERCULOSIS | SUSCEPTIBILITY | MICROBIOLOGY | IMMUNOLOGY | POLYMORPHISMS | IMMITIS | RESISTANCE | PATIENT | ASSOCIATION | Interleukin-12 - genetics | Humans | Drug Resistance, Bacterial | Male | Interferon-gamma - metabolism | Mycobacterium Infections - immunology | Antifungal Agents - therapeutic use | Young Adult | Anti-Bacterial Agents - therapeutic use | Genes, Dominant | Mycobacterium Infections - genetics | Treatment Failure | Coccidioidomycosis - drug therapy | Interferon-gamma - genetics | Drug Resistance, Fungal | Receptors, Interferon - genetics | Antifungal Agents - pharmacology | Genetic Predisposition to Disease - genetics | Receptors, Interferon - deficiency | Interleukin-12 - metabolism | Mycobacterium Infections - drug therapy | Coccidioidomycosis - genetics | Anti-Bacterial Agents - pharmacology | Immunocompromised Host | Mutation | Coccidioidomycosis - immunology
AUTOANTIBODIES | INFECTIOUS DISEASES | INFECTIONS | IFN-GAMMA | TUBERCULOSIS | SUSCEPTIBILITY | MICROBIOLOGY | IMMUNOLOGY | POLYMORPHISMS | IMMITIS | RESISTANCE | PATIENT | ASSOCIATION | Interleukin-12 - genetics | Humans | Drug Resistance, Bacterial | Male | Interferon-gamma - metabolism | Mycobacterium Infections - immunology | Antifungal Agents - therapeutic use | Young Adult | Anti-Bacterial Agents - therapeutic use | Genes, Dominant | Mycobacterium Infections - genetics | Treatment Failure | Coccidioidomycosis - drug therapy | Interferon-gamma - genetics | Drug Resistance, Fungal | Receptors, Interferon - genetics | Antifungal Agents - pharmacology | Genetic Predisposition to Disease - genetics | Receptors, Interferon - deficiency | Interleukin-12 - metabolism | Mycobacterium Infections - drug therapy | Coccidioidomycosis - genetics | Anti-Bacterial Agents - pharmacology | Immunocompromised Host | Mutation | Coccidioidomycosis - immunology
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Loading RightsJournal of Experimental Medicine, ISSN 0022-1007, 06/2010, Volume 207, Issue 6, pp. 1283 - 1292
Human BDCA3(+) dendritic cells (DCs) were suggested to be homologous to mouse CD8 alpha(+) DCs. We demonstrate that human BDCA3(+) DCs are more efficient than...
B-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | NATURAL-KILLER-CELLS | C-TYPE LECTIN | IFN-GAMMA | IN-VIVO | SUBSETS | IMMUNOLOGY | CD8(+) T-CELLS | VIRAL-INFECTION | CUTTING EDGE | ANTIGEN
B-CELLS | MEDICINE, RESEARCH & EXPERIMENTAL | NATURAL-KILLER-CELLS | C-TYPE LECTIN | IFN-GAMMA | IN-VIVO | SUBSETS | IMMUNOLOGY | CD8(+) T-CELLS | VIRAL-INFECTION | CUTTING EDGE | ANTIGEN
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Loading RightsImmunity, ISSN 1074-7613, 12/2012, Volume 37, Issue 6, pp. 1091 - 1103
Differentiation of naive CD4 T cells into T helper (Th) cells is a defining event in adaptive immunity. The cytokines and transcription factors that control Th...
EFFECTOR | DENDRITIC CELLS | IFN-GAMMA | IN-VIVO | INFECTION | IMMUNOLOGY | EXPRESSION | T-CELLS | CLASS-II | LYMPHOCYTES | ANTIGEN | Chemokines, CXC - immunology | Dendritic Cells - immunology | Lymphocytic Choriomeningitis - immunology | Th1 Cells - immunology | Lymphocytic Choriomeningitis - metabolism | Lymphocyte Activation - genetics | Lymphocyte Activation - immunology | Chemokine CXCL10 - immunology | Dendritic Cells - metabolism | Receptors, CXCR3 - metabolism | Gene Expression Regulation | Lymph Nodes - metabolism | Mice, Transgenic | Chemokine CXCL9 - immunology | Lymph Nodes - immunology | Chemokines, CXC - genetics | DNA-Binding Proteins - genetics | Chemokine CXCL9 - genetics | Cell Differentiation - immunology | Animals | Chemokine CXCL10 - genetics | Receptors, CXCR3 - genetics | Protein Binding | Ligands | Mice | Th1 Cells - cytology | Cytokines - biosynthesis | Interferon-gamma - biosynthesis | Transcription factors | Cytokines | Rodents | T cell receptors | Software | Chemokines | Immune system
EFFECTOR | DENDRITIC CELLS | IFN-GAMMA | IN-VIVO | INFECTION | IMMUNOLOGY | EXPRESSION | T-CELLS | CLASS-II | LYMPHOCYTES | ANTIGEN | Chemokines, CXC - immunology | Dendritic Cells - immunology | Lymphocytic Choriomeningitis - immunology | Th1 Cells - immunology | Lymphocytic Choriomeningitis - metabolism | Lymphocyte Activation - genetics | Lymphocyte Activation - immunology | Chemokine CXCL10 - immunology | Dendritic Cells - metabolism | Receptors, CXCR3 - metabolism | Gene Expression Regulation | Lymph Nodes - metabolism | Mice, Transgenic | Chemokine CXCL9 - immunology | Lymph Nodes - immunology | Chemokines, CXC - genetics | DNA-Binding Proteins - genetics | Chemokine CXCL9 - genetics | Cell Differentiation - immunology | Animals | Chemokine CXCL10 - genetics | Receptors, CXCR3 - genetics | Protein Binding | Ligands | Mice | Th1 Cells - cytology | Cytokines - biosynthesis | Interferon-gamma - biosynthesis | Transcription factors | Cytokines | Rodents | T cell receptors | Software | Chemokines | Immune system
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Loading RightsImmunity, ISSN 1074-7613, 09/2013, Volume 39, Issue 3, pp. 454 - 469
Synergistic activation of inflammatory cytokine genes by interferon-γ (IFN-γ) and Toll-like receptor (TLR) signaling is important for innate immunity and...
TRANSCRIPTION FACTORS | PATHWAYS | HUMAN GENOME | JAK-STAT | LANDSCAPE | IFN-GAMMA | AUTOIMMUNE-DISEASES | MECHANISMS | IMMUNOLOGY | ENHANCERS | MACROPHAGE ACTIVATION | Interleukin-12 Subunit p40 - metabolism | Promoter Regions, Genetic | Cytokines - metabolism | Signal Transduction | Humans | Cells, Cultured | Tumor Necrosis Factors - metabolism | Chromatin Assembly and Disassembly | Interferon-gamma - metabolism | Janus Kinases - antagonists & inhibitors | Macrophages - metabolism | STAT1 Transcription Factor - metabolism | Protein Binding | RNA Polymerase II - genetics | Transcription, Genetic | Acetylation | Enzyme Activation | Histones - metabolism | Toll-Like Receptors - metabolism | Interleukin-6 - metabolism | Interferon Regulatory Factor-1 - metabolism
TRANSCRIPTION FACTORS | PATHWAYS | HUMAN GENOME | JAK-STAT | LANDSCAPE | IFN-GAMMA | AUTOIMMUNE-DISEASES | MECHANISMS | IMMUNOLOGY | ENHANCERS | MACROPHAGE ACTIVATION | Interleukin-12 Subunit p40 - metabolism | Promoter Regions, Genetic | Cytokines - metabolism | Signal Transduction | Humans | Cells, Cultured | Tumor Necrosis Factors - metabolism | Chromatin Assembly and Disassembly | Interferon-gamma - metabolism | Janus Kinases - antagonists & inhibitors | Macrophages - metabolism | STAT1 Transcription Factor - metabolism | Protein Binding | RNA Polymerase II - genetics | Transcription, Genetic | Acetylation | Enzyme Activation | Histones - metabolism | Toll-Like Receptors - metabolism | Interleukin-6 - metabolism | Interferon Regulatory Factor-1 - metabolism
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Loading RightsAnnual Review of Immunology, ISSN 0732-0582, 2009, Volume 27, Issue 1, pp. 519 - 550
More than any other cytokine family, the interleukin (IL)-1 family is closely linked to the innate immune response. This linkage became evident upon the...
Inflammasome | Host defense | Autoinflammatory | Cytokine | Caspase-1 | cytokine | RHEUMATOID-ARTHRITIS | COLLAGEN-INDUCED ARTHRITIS | MICE DEFICIENT | IFN-GAMMA | host defense | TOLL-LIKE RECEPTOR | IL-1 RECEPTOR | IMMUNOLOGY | BLOOD MONONUCLEAR-CELLS | RECEPTOR ACCESSORY PROTEIN | MESSENGER-RNA | inflammasome | autoinflammatory | caspase-1 | NF-KAPPA-B | Interleukin-1 - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 1 - metabolism | Caspase 1 - immunology | Signal Transduction - immunology | Inflammation - metabolism | T-Lymphocytes, Helper-Inducer - immunology | Interleukin-1 - immunology | Toll-Like Receptors - metabolism | Receptors, Purinergic P2 - immunology | B-Lymphocytes - metabolism | Carrier Proteins - immunology | Interleukin-1 - metabolism | T-Lymphocytes, Helper-Inducer - metabolism | Receptors, Interleukin-1 - immunology | Toll-Like Receptors - immunology | Inflammation - immunology | Immunity, Innate | Receptors, Interleukin-1 - metabolism | Receptors, Purinergic P2X7 | Animals | B-Lymphocytes - immunology | Carrier Proteins - metabolism | Receptors, Purinergic P2 - metabolism | Immune response | Interleukins | Properties | Immunological research
Inflammasome | Host defense | Autoinflammatory | Cytokine | Caspase-1 | cytokine | RHEUMATOID-ARTHRITIS | COLLAGEN-INDUCED ARTHRITIS | MICE DEFICIENT | IFN-GAMMA | host defense | TOLL-LIKE RECEPTOR | IL-1 RECEPTOR | IMMUNOLOGY | BLOOD MONONUCLEAR-CELLS | RECEPTOR ACCESSORY PROTEIN | MESSENGER-RNA | inflammasome | autoinflammatory | caspase-1 | NF-KAPPA-B | Interleukin-1 - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Caspase 1 - metabolism | Caspase 1 - immunology | Signal Transduction - immunology | Inflammation - metabolism | T-Lymphocytes, Helper-Inducer - immunology | Interleukin-1 - immunology | Toll-Like Receptors - metabolism | Receptors, Purinergic P2 - immunology | B-Lymphocytes - metabolism | Carrier Proteins - immunology | Interleukin-1 - metabolism | T-Lymphocytes, Helper-Inducer - metabolism | Receptors, Interleukin-1 - immunology | Toll-Like Receptors - immunology | Inflammation - immunology | Immunity, Innate | Receptors, Interleukin-1 - metabolism | Receptors, Purinergic P2X7 | Animals | B-Lymphocytes - immunology | Carrier Proteins - metabolism | Receptors, Purinergic P2 - metabolism | Immune response | Interleukins | Properties | Immunological research
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Loading RightsNature Immunology, ISSN 1529-2908, 2013, Volume 14, Issue 5, pp. 480 - 488
NOD2 receptor and the cytosolic protein kinase RIPK2 regulate NF-kappaB and MAP kinase signaling during bacterial infections, but the role of this immune axis...
LISTERIA-MONOCYTOGENES | IMMUNE-RESPONSE | 1918 INFLUENZA-VIRUS | DOUBLE-STRANDED-RNA | IFN-GAMMA PRODUCTION | DENDRITIC CELLS | IL-1-BETA PRODUCTION | INNATE | AUTOPHAGY | IMMUNOLOGY | CD8(+) T-CELLS | Immune response | Influenza | Physiological aspects | Causes of | Genetic aspects | Cellular signal transduction | Research | Protein kinases | mitophagy | autophagy | RIPK2 | NLR | inflammasome | IL-18 | Caspase-1
LISTERIA-MONOCYTOGENES | IMMUNE-RESPONSE | 1918 INFLUENZA-VIRUS | DOUBLE-STRANDED-RNA | IFN-GAMMA PRODUCTION | DENDRITIC CELLS | IL-1-BETA PRODUCTION | INNATE | AUTOPHAGY | IMMUNOLOGY | CD8(+) T-CELLS | Immune response | Influenza | Physiological aspects | Causes of | Genetic aspects | Cellular signal transduction | Research | Protein kinases | mitophagy | autophagy | RIPK2 | NLR | inflammasome | IL-18 | Caspase-1
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