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Nature immunology, ISSN 1529-2916, 2012, Volume 13, Issue 5, pp. 449 - 456
Intestinal phagocytes transport oral antigens and promote immune tolerance, but their role in innate immune responses remains unclear. Here we found that... 
FLAGELLIN | PATTERN-RECOGNITION | NOD-LIKE RECEPTORS | ACTIVATES CASPASE-1 | MACROPHAGES | INTERLEUKIN-1-BETA | INFLAMMASOME RECEPTORS | INFECTION | NLRP3 INFLAMMASOME | SECRETION | IMMUNOLOGY | Inflammasomes - metabolism | Humans | Receptors, Interleukin-1 - genetics | Salmonella Infections - genetics | Salmonella Infections - immunology | Clonal Anergy | Caspase 1 - metabolism | Monocytes - metabolism | Monocytes - immunology | Intestines - immunology | Host-Pathogen Interactions - immunology | Signal Transduction - immunology | Calcium-Binding Proteins - immunology | Interleukin-1beta - metabolism | Tumor Necrosis Factor-alpha - immunology | Apoptosis Regulatory Proteins - genetics | Pseudomonas - immunology | Toll-Like Receptors - metabolism | Neutrophil Infiltration - immunology | Neutrophils - pathology | Apoptosis Regulatory Proteins - immunology | Flagellin - immunology | Receptors, Interleukin-1 - immunology | Mice, Inbred C57BL | Toll-Like Receptors - immunology | Neutrophils - immunology | Salmonella - genetics | Signal Transduction - genetics | Phagocytes - immunology | Neutrophil Infiltration - genetics | Mice, Knockout | Pseudomonas Infections - immunology | Salmonella - immunology | Animals | Intestines - microbiology | Phagocytes - microbiology | Inflammasomes - immunology | Interleukin-6 - immunology | Interleukin-6 - biosynthesis | Mice | Mice, Inbred BALB C | Tumor Necrosis Factor-alpha - biosynthesis | Calcium-Binding Proteins - genetics
Journal Article
Nature immunology, ISSN 1529-2916, 2012, Volume 14, Issue 2, pp. 162 - 171
Signaling through the G protein-coupled receptors for the complement fragments C3a and C5a (C3aR and C5aR, respectively) by dendritic cells and CD4(+) cells... 
Forkhead Transcription Factors - immunology | Cell Communication - immunology | T-Lymphocytes, Regulatory - metabolism | TOR Serine-Threonine Kinases - metabolism | Transforming Growth Factor beta1 - metabolism | Complement C5a - metabolism | Receptors, Complement - metabolism | T-Lymphocytes, Regulatory - immunology | Signal Transduction - immunology | Transforming Growth Factor beta1 - immunology | Forkhead Transcription Factors - metabolism | Class Ib Phosphatidylinositol 3-Kinase - metabolism | T-Lymphocytes, Regulatory - cytology | Interleukin-10 - metabolism | Receptor, Anaphylatoxin C5a - immunology | Cell Differentiation | Proto-Oncogene Proteins c-akt - metabolism | Complement C3a - metabolism | Interleukin-6 - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Receptors, Chemokine - metabolism | Gene Expression Regulation | Mice, Transgenic | Receptors, Chemokine - immunology | Receptor Cross-Talk - immunology | TOR Serine-Threonine Kinases - immunology | Animals | Proto-Oncogene Proteins c-akt - immunology | Receptors, Complement - immunology | Cyclic AMP-Dependent Protein Kinases - immunology | Interleukin-6 - immunology | Mice | Complement C3a - immunology | Complement C5a - immunology | Class Ib Phosphatidylinositol 3-Kinase - immunology | Interleukin-10 - immunology | Receptor, Anaphylatoxin C5a - metabolism
Journal Article
The Journal of immunology (1950), ISSN 1550-6606, 2009, Volume 183, Issue 8, pp. 4895 - 4903
The definitions of tolerogenic vs immunogenic dendritic cells (DC) remain controversial. Immature DC have been shown to induce T regulatory cells (Treg)... 
MULTIPLE-MYELOMA | NOD MICE | TGF-BETA | DENDRITIC CELLS | NONOBESE DIABETIC MICE | TOLERANCE | IN-VIVO | HORROR AUTOTOXICUS | IMMUNOLOGY | DE-NOVO DIFFERENTIATION | PEPTIDE | Forkhead Transcription Factors - immunology | T-Lymphocytes, Regulatory - metabolism | Dose-Response Relationship, Immunologic | Ovalbumin - immunology | Phosphotransferases (Alcohol Group Acceptor) - immunology | Coculture Techniques | Dendritic Cells - immunology | CD28 Antigens - metabolism | T-Lymphocytes, Regulatory - immunology | CD4-Positive T-Lymphocytes - immunology | Signal Transduction - immunology | Antibodies - immunology | Receptors, Antigen, T-Cell - immunology | Diabetes Mellitus, Type 1 - immunology | Oncogene Protein v-akt - metabolism | Interleukin-6 - metabolism | Carrier Proteins - immunology | Dendritic Cells - metabolism | Cytokines - immunology | Interleukin-6 - genetics | Receptors, Antigen, T-Cell - metabolism | Mice, Inbred C57BL | Peptides - immunology | CD4-Positive T-Lymphocytes - metabolism | CD28 Antigens - immunology | CD3 Complex - metabolism | Mice, Knockout | Phosphotransferases (Alcohol Group Acceptor) - metabolism | CD3 Complex - drug effects | CD28 Antigens - drug effects | Animals | Carrier Proteins - metabolism | CD3 Complex - immunology | Interleukin-6 - immunology | Antigens - immunology | Mice, Inbred NOD | Oncogene Protein v-akt - immunology | Mice | Mice, Inbred BALB C | TOR Serine-Threonine Kinases | Cytokines - biosynthesis
Journal Article
Immunity (Cambridge, Mass.), ISSN 1074-7613, 2015, Volume 43, Issue 3, pp. 475 - 487
Interleukin-17 (IL-17) induces pathology in autoimmunity and infections; therefore, constraint of this pathway is an essential component of its regulation. We... 
negative regulation | Regnase-1 | fungal immunity | autoimmunity | signal transduction | IL-17 | Autoimmunity | Signal transduction | Fungal immunity | Negative regulation | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | IL-17 RECEPTOR | TARGET GENES | CANDIDA-ALBICANS | C/EBP-BETA | GENE-EXPRESSION | HOST-DEFENSE | NECROSIS-FACTOR-ALPHA | MESSENGER-RNA STABILITY | T-CELL | IMMUNOLOGY | Candidiasis - genetics | Oncogene Proteins - genetics | Humans | Encephalomyelitis, Autoimmune, Experimental - immunology | Immunoblotting | Male | Receptors, Interleukin-17 - genetics | Ribonucleases - metabolism | Host-Pathogen Interactions - immunology | Inflammation - metabolism | Lipocalins - genetics | Adaptor Proteins, Signal Transducing - immunology | Pneumonia - immunology | Candida albicans - physiology | Encephalomyelitis, Autoimmune, Experimental - genetics | Receptors, Interleukin-17 - metabolism | Interleukin-6 - metabolism | Pneumonia - genetics | Interleukin-6 - genetics | Oncogene Proteins - metabolism | Signal Transduction - genetics | Candida albicans - immunology | Reverse Transcriptase Polymerase Chain Reaction | Mice, Knockout | Interleukin-17 - metabolism | Lipocalin-2 | Lipocalins - immunology | Interleukin-6 - immunology | Pneumonia - metabolism | Ribonucleases - genetics | Encephalomyelitis, Autoimmune, Experimental - metabolism | Receptors, Interleukin-17 - immunology | Interleukin-17 - immunology | Acute-Phase Proteins - genetics | Candidiasis - microbiology | Signal Transduction - immunology | HEK293 Cells | Female | Candidiasis - immunology | Nuclear Proteins - genetics | Oncogene Proteins - immunology | Lipocalins - metabolism | Cell Line | Acute-Phase Proteins - metabolism | Mice, Inbred C57BL | Cells, Cultured | Nuclear Proteins - metabolism | Inflammation - immunology | Nuclear Proteins - immunology | Animals | Ribonucleases - immunology | Adaptor Proteins, Signal Transducing - genetics | Inflammation - genetics | Adaptor Proteins, Signal Transducing - metabolism | Acute-Phase Proteins - immunology | Medical colleges | Nucleases | Interleukins | RNA | Cellular signal transduction | Inflammation | Proteins | Cytokines | Rodents | Fibroblasts | Infections | Kinases | Laboratory animals | Gene expression | Experiments
Journal Article
Nature communications, ISSN 2041-1723, 2011, Volume 2, Issue 1, p. 240
The immune system can both promote and suppress cancer. Chronic inflammation and proinflammatory cytokines such as interleukin (IL)-1 and IL-6 are considered... 
LUNG-CANCER | INTERFERON-INDUCIBLE PROTEIN-10 | NECROSIS IN-VIVO | PROGNOSTIC-FACTORS | INTERLEUKIN-1 RECEPTOR ANTAGONIST | IFN-GAMMA | MULTIDISCIPLINARY SCIENCES | CD4(+) T-CELLS | ADJUVANT THERAPY | CARCINOMA | EXPRESSION | Angiostatic Proteins - immunology | Immunohistochemistry | Neoplasms - metabolism | Interleukin-1alpha - immunology | Chemokine CXCL9 - biosynthesis | Tumor Microenvironment | Multiple Myeloma - immunology | Th2 Cells - immunology | Th1 Cells - immunology | CD4-Positive T-Lymphocytes - immunology | Chemokine CXCL10 - biosynthesis | Inflammation - metabolism | Interleukin-2 - immunology | Chemokine CXCL10 - immunology | Lymphoma, B-Cell - immunology | Interleukin-1beta - biosynthesis | Macrophages - immunology | Interleukin-12 - biosynthesis | Lymphoma, B-Cell - metabolism | Signal Transduction | Angiostatic Proteins - biosynthesis | CD4-Positive T-Lymphocytes - cytology | CD4-Positive T-Lymphocytes - metabolism | Interleukin-1beta - immunology | Chemokine CXCL9 - immunology | Inflammation - immunology | Macrophages - cytology | Mice, SCID | Multiple Myeloma - metabolism | Macrophages - metabolism | Multiple Myeloma - pathology | Animals | Neoplasms - immunology | Interferon-gamma - immunology | Interleukin-12 - immunology | Interleukin-6 - immunology | Lymphoma, B-Cell - pathology | Cell Line, Tumor | Interleukin-6 - biosynthesis | Interleukin-1alpha - biosynthesis | Mice | Interleukin-2 - biosynthesis | Neoplasms - pathology | Interferon-gamma - biosynthesis
Journal Article
The Journal of immunology (1950), ISSN 1550-6606, 2009, Volume 183, Issue 8, pp. 5208 - 5220
The role of proinflammatory cytokine production in the pathogenesis of malaria is well established, but the identification of the parasite products that... 
TUMOR-NECROSIS-FACTOR | DENDRITIC CELLS | INTERFERON-GAMMA | TOLL-LIKE RECEPTOR-9 | PLASMODIUM-FALCIPARUM | EXPERIMENTAL CEREBRAL MALARIA | ENDOTHELIAL-CELLS | IMMUNOLOGY | NF-KAPPA-B | INNATE IMMUNE ACTIVATION | INTRACELLULAR COMPARTMENTS | Interleukin-1alpha - immunology | Chemokine CCL2 - immunology | NLR Family, Pyrin Domain-Containing 3 Protein | NF-kappa B - metabolism | Inflammation - parasitology | Endothelial Cells - parasitology | Extracellular Signal-Regulated MAP Kinases - immunology | Plasmodium falciparum | Interleukin-1beta - metabolism | Tumor Necrosis Factor-alpha - immunology | Interleukin-8 - metabolism | Toll-Like Receptors - metabolism | Chemokine CXCL1 - metabolism | Interleukin-6 - metabolism | Carrier Proteins - immunology | Toll-Like Receptors - immunology | Chemokine CXCL1 - immunology | Signal Transduction - drug effects | Interleukin-6 - immunology | Malaria, Falciparum - immunology | Uric Acid - antagonists & inhibitors | Mice | Interleukin-8 - immunology | Inflammation - chemically induced | Tumor Necrosis Factor-alpha - metabolism | NF-kappa B - immunology | Interleukin-1alpha - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Hemeproteins - immunology | Macrophages - parasitology | Signal Transduction - immunology | Myeloid Differentiation Factor 88 - immunology | Cytoskeletal Proteins - metabolism | Chemokine CCL2 - metabolism | Macrophages - immunology | Uric Acid - metabolism | Interleukin-1beta - immunology | Hemeproteins - pharmacology | Inflammation - immunology | Endothelial Cells - immunology | Malaria, Falciparum - parasitology | Animals | Apoptosis Regulatory Proteins | Carrier Proteins - metabolism | Cytoskeletal Proteins - immunology | CARD Signaling Adaptor Proteins | Allopurinol - pharmacology | Macrophages - drug effects | Myeloid Differentiation Factor 88 - metabolism | Interferon-gamma - pharmacology | Endothelial Cells - drug effects | Chemokine | TLR9 | Plasmodium | Inflammasome | NALP3 | Cytokine
Journal Article
Arthritis research & therapy, ISSN 1478-6354, 2013, Volume 15, Issue 5, pp. R168 - R168
Introduction: B lymphocytes might play a pathogenic role in dermal fibrosis in systemic sclerosis (SSc). B-cell activating factor (BAFF), a key cytokine for... 
BAFF | ADHESION | SCLERODERMA | TIMP-1 | AUTOIMMUNITY | SKIN FIBROSIS | DEPLETION | MECHANISMS | RHEUMATOLOGY | INTERLEUKIN-6 | IL-6 | Gene Expression - drug effects | Chemokine CCL2 - immunology | Skin - metabolism | Antibodies, Anti-Idiotypic - pharmacology | Coculture Techniques | Humans | Transforming Growth Factor beta1 - metabolism | Actins - metabolism | Matrix Metalloproteinase 9 - immunology | Fibrosis - metabolism | Actins - immunology | Immunoglobulin M - immunology | Actins - genetics | Transforming Growth Factor beta1 - immunology | Matrix Metalloproteinase 9 - genetics | Fibrosis - immunology | Gene Expression - immunology | B-Cell Activating Factor - immunology | Chemokine CCL2 - metabolism | Collagen - genetics | Interleukin-6 - metabolism | B-Lymphocytes - metabolism | Skin - pathology | Fibroblasts - metabolism | Skin - immunology | B-Lymphocytes - cytology | Fibrosis - genetics | Enzyme-Linked Immunosorbent Assay | Collagen - immunology | Scleroderma, Systemic - metabolism | Cells, Cultured | Scleroderma, Systemic - genetics | Antibodies, Anti-Idiotypic - immunology | Scleroderma, Systemic - immunology | Fibroblasts - pathology | Reverse Transcriptase Polymerase Chain Reaction | Muscle, Smooth - chemistry | Collagen - metabolism | Tissue Inhibitor of Metalloproteinase-1 - genetics | B-Cell Activating Factor - metabolism | B-Lymphocytes - immunology | Interleukin-6 - immunology | Fibroblasts - immunology | B-Cell Activating Factor - pharmacology | Tissue Inhibitor of Metalloproteinase-1 - immunology | Computer software industry | Cytokines | RNA | Systemic scleroderma | Scleroderma (Disease) | Fibroblasts | Bone morphogenetic proteins | B cells | Transforming growth factors | Blood donors | Life Sciences | Human health and pathology | Rhumatology and musculoskeletal system
Journal Article
Nature medicine, ISSN 1546-170X, 2016, Volume 22, Issue 9, pp. 1013 - 1022
Mechanisms by which regulatory T (Treg) cells fail to control inflammation in asthma remain poorly understood. We show that a severe asthma-associated... 
GRB2 Adaptor Protein - immunology | Immunoprecipitation | Humans | Middle Aged | Interleukin-17 - immunology | Interleukin-13 - immunology | Immunoblotting | Male | Gene Expression Profiling | Case-Control Studies | Interleukin-4 Receptor alpha Subunit - genetics | T-Lymphocytes, Regulatory - immunology | Young Adult | Th17 Cells - drug effects | Flow Cytometry | Asthma - immunology | Adult | Female | Receptors, Interleukin-6 - immunology | Child | Real-Time Polymerase Chain Reaction | Nuclear Receptor Subfamily 1, Group F, Member 3 - genetics | Disease Models, Animal | Nuclear Receptor Subfamily 1, Group F, Member 3 - immunology | Receptors, Interleukin-6 - genetics | Antibodies, Neutralizing - pharmacology | Inflammation - immunology | Respiratory Hypersensitivity - immunology | Reverse Transcriptase Polymerase Chain Reaction | Interleukin-4 Receptor alpha Subunit - immunology | Asthma - genetics | Polymorphism, Genetic | Cell Differentiation - immunology | T-Lymphocytes, Regulatory - drug effects | Animals | Cell Differentiation - drug effects | Adolescent | Interleukin-6 - immunology | Th17 Cells - immunology | Mice | STAT3 Transcription Factor - immunology | Lung - immunology | Receptors, Cell Surface - genetics | Complications and side effects | Airway obstruction (Medicine) | T cells | Analysis | Risk factors | Asthma | Airway management | Inflammatory diseases | Cells
Journal Article
Clinical infectious diseases, ISSN 1537-6591, 2015, Volume 61, Issue 2, pp. 260 - 269
Background. Women in Africa, especially young women, have very high human immunodeficiency virus (HIV) incidence rates that cannot be fully explained by... 
cytokine | female genital tract | inflammation | HIV transmission | INFECTIOUS DISEASES | METAANALYSIS | RANTES | TRACT INFLAMMATION |