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1. Full Text Cortical Astrocytes Acutely Exposed to the Monomethylarsonous Acid (MMAIII) Show Increased Pro-inflammatory Cytokines Gene Expression that is Consistent with APP and BACE-1: Over-expression
by Escudero-Lourdes, C and Uresti-Rivera, E E and Oliva-González, C and Torres-Ramos, M A and Aguirre-Bañuelos, P and Gandolfi, A J
Neurochemical Research, ISSN 0364-3190, 10/2016, Volume 41, Issue 10, pp. 2559 - 2572
Long-term exposure to inorganic arsenic (iAs) through drinking water has been associated with cognitive impairment in children and adults; however, the related... 
Neurochemistry | Biochemistry, general | Neurology | APP | Neurosciences | Biomedicine | Arsenic | Astrocytes | BACE-1 | Inflammation | Cognitive | Cell Biology | ARSENIC EXPOSURE | OXIDATIVE DNA-DAMAGE | ALZHEIMERS-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | COGNITIVE IMPAIRMENT | ADULT-RATS | AMYLOID PRECURSOR PROTEIN | SODIUM ARSENITE | PRIMARY CULTURES | NEUROSCIENCES | A-BETA | YOUNG-RATS | Astrocytes - drug effects | Cell Line | Cell Survival - drug effects | Cytokines - metabolism | Rats, Wistar | Cells, Cultured | Gene Expression Regulation - drug effects | Amyloid Precursor Protein Secretases - metabolism | Animals | Aspartic Acid Endopeptidases - metabolism | Amyloid beta-Protein Precursor - metabolism | Homeostasis - drug effects | Cytokines - genetics | Organometallic Compounds - pharmacology | Cytokines | Metabolites | Genes | Amyloid beta-protein | Gene expression
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2. Full Text Erratum to: Cortical Astrocytes Acutely Exposed to the Monomethylarsonous Acid (MMAIII) Show Increased Pro-inflammatory Cytokines Gene Expression that is Consistent with APP and BACE-1 Over-expression
by Escudero-Lourdes, C and Uresti-Rivera, E E and Oliva-González, C and Torres-Ramos, M A and Aguirre-Bañuelos, P and Gandolfi, A J
Neurochemical Research, ISSN 0364-3190, 10/2016, Volume 41, Issue 10, pp. 2573 - 2573
To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1007/s11064-016-2005-y 
Neurochemistry | Biochemistry, general | Neurology | Neurosciences | Biomedicine | Cell Biology | NEUROSCIENCES | BIOCHEMISTRY & MOLECULAR BIOLOGY | Cytokines | Gene expression | Pharmacy
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3. Full Text Short-term treatment of RAW264.7 macrophages with adiponectin increases tumor necrosis factor-α (TNF-α) expression via ERK1/2 activation and Egr-1 expression: Role of TNF-α in adiponectin-stimulated interleukin-10 production
by Park, Pil-Hoon and McMullen, Megan R and Huang, Honglian and Thakur, Varsha and Nagy, Laura E
Journal of Biological Chemistry, ISSN 0021-9258, 07/2007, Volume 282, Issue 30, pp. 21695 - 21703
Adiponectin is an adipokine with potent anti-inflammatory properties. However, the mechanisms by which adiponectin suppresses macrophage function are not well... 
TRANSCRIPTION FACTORS | RAT KUPFFER CELLS | HUMAN MONOCYTIC CELLS | PROTEIN | BIOCHEMISTRY & MOLECULAR BIOLOGY | MICE | RECEPTORS | INDUCED LIVER-INJURY | LPS | ANTIINFLAMMATORY CYTOKINES | FAMILY | Macrophages - physiology | Cell Line | Adiponectin - pharmacology | Phosphorylation | Tumor Necrosis Factor-alpha - genetics | NF-kappa B - metabolism | DNA Primers | Luciferases - genetics | Macrophages - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Early Growth Response Protein 1 - genetics | Lipopolysaccharides - pharmacology | Interleukin-10 - biosynthesis | Macrophages - drug effects | Mice | Enzyme Activation | Cytokines - biosynthesis | Genes, Reporter | Mitogen-Activated Protein Kinase 1 - metabolism
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4. Full Text Inflammation Directs Memory Precursor and Short-Lived Effector CD8 + T Cell Fates via the Graded Expression of T-bet Transcription Factor
by Joshi, Nikhil S and Cui, Weiguo and Chandele, Anmol and Lee, Heung Kyu and Urso, David R and Hagman, James and Gapin, Laurent and Kaech, Susan M
Immunity, ISSN 1074-7613, 2007, Volume 27, Issue 2, pp. 281 - 295
As acute infections resolve, effector CD8 T cells differentiate into interleukin-7 receptor (IL-7R ) short-lived effector cells (SLECs) and IL-7R memory... 
MOLIMMUNO | CELLIMMUNO | VIRAL-INFECTIONS | RESPONSES | PROTECTIVE IMMUNITY | HOMEOSTASIS | SELECTIVE EXPRESSION | IN-VIVO | IL-7 RECEPTOR | DIFFERENTIATION | IMMUNOLOGY | CUTTING EDGE | ANTIGEN | Biomarkers - metabolism | Receptors, Interleukin-7 - metabolism | Cytokines - metabolism | Infection - immunology | Biomarkers - analysis | Infection - microbiology | Infection - virology | Inflammation - immunology | Interleukin-12 - metabolism | Interferon-gamma - metabolism | Receptors, Immunologic - analysis | T-Box Domain Proteins - metabolism | Animals | Mice, Mutant Strains | Interleukin-15 - metabolism | Immunologic Memory | Mice | CD8-Positive T-Lymphocytes - immunology | Receptors, Immunologic - metabolism | Transcription factors | Bacterial infections | Peptides | Lymphocytes | T cell receptors | Gene expression | Viral infections | Immune system
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5. Full Text Increased IL-10 mRNA and IL-23 mRNA expression in multiple sclerosis: interferon-β treatment increases IL-10 mRNA expression while reducing IL-23 mRNA expression
by Krakauer, M and Sorensen, P and Khademi, M and Olsson, T and Sellebjerg, F
Multiple Sclerosis, ISSN 1352-4585, 06/2008, Volume 14, Issue 5, pp. 622 - 630
Background Interferon (IFN)-β therapy in multiple sclerosis (MS) has been suggested to promote a deviation from T lymphocyte production of pathogenic Th1... 
Multiple sclerosis | Cytokines | Interleukin-10 | Immunotherapy | Interferon-β treatment | Interleukin-23 | Autoimmune diseases | autoimmune diseases | GAMMA | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | multiple sclerosis | MONONUCLEAR-CELLS | DOWN-REGULATION | PERIPHERAL-BLOOD | interleukin-10 | CLINICAL NEUROLOGY | interleukin-23 | I IFNS | interferon-beta treatment | INTERLEUKIN-10 EXPRESSION | INFLAMMATION | immunotherapy | cytokines | T-CELLS | Biomarkers - metabolism | Th1 Cells - drug effects | Th1 Cells - physiology | Multiple Sclerosis, Relapsing-Remitting - immunology | Th2 Cells - physiology | Gene Expression - drug effects | Multiple Sclerosis, Relapsing-Remitting - drug therapy | Humans | Multiple Sclerosis, Relapsing-Remitting - physiopathology | Transcription Factors - genetics | RNA, Messenger - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Th2 Cells - drug effects | Interleukin-23 - immunology | Interferon-beta - therapeutic use | Interleukin-23 - genetics | Interleukin-10 - genetics | Gene Expression - immunology | Interleukin-10 - immunology | Immunologic Factors - therapeutic use
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6. Full Text Luteolin downregulates TLR4, TLR5, NF-κB and p-p38MAPK expression, upregulates the p-ERK expression, and protects rat brains against focal ischemia
by Qiao, Huimin and Zhang, Xiangjian and Zhu, Chunhua and Dong, Lipeng and Wang, Lina and Zhang, Xiaolin and Xing, Yinxue and Wang, Chaohui and Ji, Ye and Cao, Xiaoyun
Brain Research, ISSN 0006-8993, 2012, Volume 1448, pp. 71 - 81
Abstract Background Inflammatory damage is known to be involved in ischemic stroke. Luteolin has been proved to elicit a series of biologic effects through its... 
Neurology | Neuroprotection | Inflammation | Luteolin | Ischemic stroke | SIGNALING PATHWAYS | NECROSIS-FACTOR-ALPHA | EXPERIMENTAL STROKE | MAP KINASES | NEUROSCIENCES | CEREBRAL-ARTERY OCCLUSION | TOLL-LIKE RECEPTORS | CENTRAL-NERVOUS-SYSTEM | INFLAMMATORY CYTOKINES | MOLECULAR-MECHANISMS | INNATE IMMUNITY | Immunohistochemistry | Neuroprotective Agents | Toll-Like Receptor 4 - biosynthesis | p38 Mitogen-Activated Protein Kinases - biosynthesis | Male | Cerebral Infarction - prevention & control | Extracellular Signal-Regulated MAP Kinases - genetics | Brain Edema - prevention & control | Stroke - pathology | Movement Disorders - prevention & control | Toll-Like Receptor 5 - biosynthesis | Phosphorylation - drug effects | Real-Time Polymerase Chain Reaction | Cerebral Infarction - pathology | Brain Edema - etiology | Rats | Stroke - drug therapy | Infarction, Middle Cerebral Artery - pathology | Down-Regulation - drug effects | Luteolin - pharmacology | Extracellular Signal-Regulated MAP Kinases - biosynthesis | Rats, Sprague-Dawley | Blotting, Western | Gene Expression Regulation - drug effects | Up-Regulation - drug effects | Nervous System Diseases - prevention & control | Animals | NF-kappa B - biosynthesis | Brain Ischemia - drug therapy | Movement Disorders - etiology | Brain Ischemia - pathology | Brain - pathology | Nervous System Diseases - etiology
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7. Full Text Dynamic expression profiling of type I and type III interferon‐stimulated hepatocytes reveals a stable hierarchy of gene expression
by Bolen, Christopher R and Ding, Siyuan and Robek, Michael D and Kleinstein, Steven H
Hepatology, ISSN 0270-9139, 04/2014, Volume 59, Issue 4, pp. 1262 - 1272
Despite activating similar signaling cascades, the type I and type III interferons (IFNs) differ in their ability to antagonize virus replication. However, it... 
IFN-LAMBDA | HEPATOCELLULAR-CARCINOMA CELLS | B-VIRUS | APOPTOSIS | C VIRUS-REPLICATION | ACTIVATION | CHRONIC HEPATITIS-C | ALPHA | INDUCTION | GASTROENTEROLOGY & HEPATOLOGY | IFN-ALPHA-2 | Phosphorylation | Humans | Hepatocytes - pathology | Gene Expression Profiling | Hepatocytes - metabolism | STAT1 Transcription Factor - metabolism | Time Factors | Feedback | Interferon Type I - pharmacology | Cell Line, Tumor | Gene Expression Regulation, Neoplastic - drug effects | Interleukins - pharmacology | Hepatocytes - drug effects | Medical research | Cytokines | Gene expression | Hepatology | cytokine signaling | innate immunity | interferon | liver
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8. Full Text Plasticity of Foxp3+ T Cells Reflects Promiscuous Foxp3 Expression in Conventional T Cells but Not Reprogramming of Regulatory T Cells
by Miyao, Takahisa and Floess, Stefan and Setoguchi, Ruka and Luche, Hervé and Fehling, Hans Joerg and Waldmann, Herman and Huehn, Jochen and Hori, Shohei
Immunity, ISSN 1074-7613, 02/2012, Volume 36, Issue 2, pp. 262 - 275
The emerging notion of environment-induced reprogramming of Foxp3 regulatory T (Treg) cells into helper T (Th) cells remains controversial. By genetic fate... 
TGF-BETA | DNA METHYLATION | TRANSCRIPTION FACTOR FOXP3 | IN-VIVO | GENE-EXPRESSION | IMMUNOLOGICAL SELF-TOLERANCE | MICE | INDUCTION | IMMUNOLOGY | LINEAGE | ANTIGEN | T-Lymphocyte Subsets - immunology | Inflammation - pathology | T-Lymphocytes, Regulatory - metabolism | T-Lymphocyte Subsets - cytology | Epigenesis, Genetic | Humans | CD2 Antigens - genetics | Lymphopenia - pathology | T-Lymphocytes, Regulatory - immunology | CD4-Positive T-Lymphocytes - immunology | DNA Methylation | Inflammation - metabolism | Forkhead Transcription Factors - metabolism | Lymphopenia - metabolism | T-Lymphocytes, Regulatory - cytology | CD2 Antigens - metabolism | Cell Differentiation | Cell Lineage - genetics | Gene Expression | Lymphocyte Activation | CD4-Positive T-Lymphocytes - cytology | CD4-Positive T-Lymphocytes - metabolism | Mice, Transgenic | Inflammation - immunology | Forkhead Transcription Factors - genetics | Mice, Knockout | Animals | Interleukin-2 Receptor alpha Subunit - metabolism | T-Lymphocyte Subsets - metabolism | Immunologic Memory | Lymphopenia - immunology | Mice | In Vitro Techniques | Cell Lineage - immunology | Transcription factors | Cytokines | Science | Cell division | Homeostasis | Artificial chromosomes | Proteins | Genotype & phenotype | Lymphocytes | Rodents | DNA methylation | Software | Deoxyribonucleic acid--DNA
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9. Full Text Nicotinamide downregulates gene expression of interleukin‐6, interleukin‐10, monocyte chemoattractant protein‐1, and tumour necrosis factor‐α gene expression in HaCaT keratinocytes after ultraviolet B irradiation
by Monfrecola, G and Gaudiello, F and Cirillo, T and Fabbrocini, G and Balato, A and Lembo, S
Clinical and Experimental Dermatology, ISSN 0307-6938, 03/2013, Volume 38, Issue 2, pp. 185 - 188
Ultraviolet ( UV ) radiation has profound effects on human skin, causing sunburn, inflammation, cellular‐tissue injury, cell death, and skin cancer. Most of... 
TOPICAL NICOTINAMIDE | INHIBITORS | RADIATION-INDUCED IMMUNOSUPPRESSION | DERMATOLOGY | Cytokines - metabolism | Interleukin-6 - genetics | Keratinocytes - radiation effects | Skin - metabolism | Down-Regulation | Humans | Tumor Necrosis Factor-alpha - genetics | Chemokine CCL2 - genetics | Gene Expression Profiling | RNA, Messenger - metabolism | Vitamin B Complex - pharmacology | Ultraviolet Rays | Keratinocytes - drug effects | Keratinocytes - metabolism | Skin - radiation effects | Interleukin-10 - genetics | Niacinamide - pharmacology | Real-Time Polymerase Chain Reaction | Skin - drug effects
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10. Full Text Upregulation of PD-1 expression on HIV-specific CD8 + T cells leads to reversible immune dysfunction
by Routy, Jean-Pierre and Chomont, Nicolas and Delwart, Eric and Sekaly, Rafick-Pierre and Haddad, Elias K and Balderas, Robert S and Sepulveda, Homero and Bessette, Benoit and Trautmann, Lydie and Gimmig, Sylvain and Janbazian, Loury and Said, Elias A and Boulassel, Mohamed-Rachid
Nature Medicine, ISSN 1078-8956, 10/2006, Volume 12, Issue 10, pp. 1198 - 1202
The engagement of programmed death 1 (PD-1) to its ligands, PD-L1 and PD-L2, inhibits proliferation and cytokine production mediated by antibodies to CD3... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | PERSISTENCE | BIOCHEMISTRY & MOLECULAR BIOLOGY | PERFORIN | RECEPTOR | ANTIRETROVIRAL THERAPY | PROLIFERATION | CHRONIC VIRAL-INFECTION | ESCAPE | CELL BIOLOGY | LYMPHOCYTES | ANTIGEN | Apoptosis Regulatory Proteins - biosynthesis | HIV Infections - blood | Amino Acid Sequence | Up-Regulation | Cell Proliferation | Cytokines - metabolism | Receptors, Antigen, T-Cell - metabolism | Antigens, CD - biosynthesis | Humans | Immune System Diseases - immunology | Molecular Sequence Data | Immune System - pathology | Immunophenotyping | CD3 Complex - biosynthesis | CD8-Positive T-Lymphocytes - virology | CD8-Positive T-Lymphocytes - metabolism | Programmed Cell Death 1 Receptor | Cell Differentiation | Immune System Diseases - pathology | HIV Infections - metabolism | Immunology | Inhibitor drugs | Cytokines | HIV | Human immunodeficiency virus | Gene expression | Apoptosis
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11. Full Text Yin/Yang expression of CCN family members: Transforming growth factor beta 1, via ALK5/FAK/MEK, induces CCN1 and CCN2, yet suppresses CCN3, expression in human dermal fibroblasts
by Peidl, Alexander and Perbal, Bernard and Leask, Andrew
PloS one, ISSN 1932-6203, 2019, Volume 14, Issue 6, p. e0218178
The role of the microenvironment in driving connective tissue disease is being increasingly appreciated. Matricellular proteins of the CCN family are signaling... 
Messenger RNA | Cytokines | Fibrosis | Physiological aspects | Research | Gene expression | Transforming growth factors | Cell culture | Homeostasis | Arthritis | Kinases | Tissues | Proteins | Connective tissues | Signal transduction | Alterations | Fibroblasts | Extracellular matrix | Inhibition | Growth factors | Transforming growth factor-b1 | TAK1 protein | Connective tissue diseases | Melanoma | Connective tissue growth factor | Yes-associated protein | Hypotheses | Adhesives | Pulmonary fibrosis | Antibiotics | Skin | Transduction | In vivo methods and tests | Diabetes | Focal adhesion kinase
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