NATURE IMMUNOLOGY, ISSN 1529-2908, 02/2018, Volume 19, Issue 2, pp. 173 - 173
CD8(+) T cell immunosurveillance dynamics influence the outcome of intracellular infections and cancer. Here we used two-photon intravital microscopy to...
MIGRATION | PROTECTIVE IMMUNITY | ACTIVATION | PERSISTENCE | RM CELLS | LOCAL ANTIGEN | INFECTION | DIFFERENTIATION | IMMUNOLOGY | PROLIFERATIVE CAPACITY | LYMPHOCYTES | Cell proliferation | Antigens | Memory cells | Immunological memory | CD8 antigen | Mucosa | Immunosurveillance | Activation | Lymphocytes T | Lymphoid tissue | Cell differentiation | Microscopy | Lymphocytes | Rodents | Skin | Recall | Cancer
MIGRATION | PROTECTIVE IMMUNITY | ACTIVATION | PERSISTENCE | RM CELLS | LOCAL ANTIGEN | INFECTION | DIFFERENTIATION | IMMUNOLOGY | PROLIFERATIVE CAPACITY | LYMPHOCYTES | Cell proliferation | Antigens | Memory cells | Immunological memory | CD8 antigen | Mucosa | Immunosurveillance | Activation | Lymphocytes T | Lymphoid tissue | Cell differentiation | Microscopy | Lymphocytes | Rodents | Skin | Recall | Cancer
Journal Article
Immunology, ISSN 0019-2805, 11/2009, Volume 128, Issue 3, pp. 311 - 323
Summary Toll‐like receptors (TLR) play a central role in the initiation of the innate immune response to pathogens. Upon recognition of molecular motifs...
viruses | B cells | bacteria | Toll‐like receptors | antibody responses | Toll-like receptors | Bacteria | Viruses | Antibody responses | PROLIFERATIVE RESPONSES | INDUCED CYTIDINE DEAMINASE | IMMUNOLOGY | CPG DNA | C-H TRANSCRIPTION | BLOOD MONONUCLEAR-CELLS | PLASMACYTOID DENDRITIC CELLS | INFLUENZA-VIRUS INFECTION | CLASS-SWITCH RECOMBINATION | NF-KAPPA-B | BRUTONS-TYROSINE KINASE | Immunomodulation | Humans | Toll-Like Receptors - immunology | Immunity, Innate | Host-Pathogen Interactions | Animals | Toll-Like Receptors - genetics | Antibody Formation | Mice | B-Lymphocytes - pathology | Toll-Like Receptors - metabolism | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Antigens | Immunoglobulins | Universities and colleges | Review
viruses | B cells | bacteria | Toll‐like receptors | antibody responses | Toll-like receptors | Bacteria | Viruses | Antibody responses | PROLIFERATIVE RESPONSES | INDUCED CYTIDINE DEAMINASE | IMMUNOLOGY | CPG DNA | C-H TRANSCRIPTION | BLOOD MONONUCLEAR-CELLS | PLASMACYTOID DENDRITIC CELLS | INFLUENZA-VIRUS INFECTION | CLASS-SWITCH RECOMBINATION | NF-KAPPA-B | BRUTONS-TYROSINE KINASE | Immunomodulation | Humans | Toll-Like Receptors - immunology | Immunity, Innate | Host-Pathogen Interactions | Animals | Toll-Like Receptors - genetics | Antibody Formation | Mice | B-Lymphocytes - pathology | Toll-Like Receptors - metabolism | Immunoglobulin Class Switching | B-Lymphocytes - metabolism | Antigens | Immunoglobulins | Universities and colleges | Review
Journal Article
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Full Text
Defective immune responses in mice lacking LUBAC‐mediated linear ubiquitination in B cells
The EMBO Journal, ISSN 0261-4189, 09/2013, Volume 32, Issue 18, pp. 2463 - 2476
The linear ubiquitin chain assembly complex (LUBAC) plays a crucial role in activating the canonical NF‐κB pathway, which is important for B‐cell development...
B cell | linear ubiquitin chain assembly complex | antibody response | canonical NF‐κB pathway | ERK | Canonical NF-κB pathway | Linear ubiquitin chain assembly complex | Antibody response | ACTIVATION | COMPLEX | INDEPENDENT TYPE-2 ANTIGENS | BIOCHEMISTRY & MOLECULAR BIOLOGY | canonical NF-kappa B pathway | RECEPTOR | CELL BIOLOGY | CHRONIC PROLIFERATIVE DERMATITIS | LYMPHOCYTE DEVELOPMENT | SIGNALING PATHWAY | CHAINS | NF-KAPPA-B | NEMO | Immunity, Cellular - genetics | Electrophoresis, Polyacrylamide Gel | Mice, Inbred C57BL | NF-kappa B - immunology | Immunoblotting | Mice, Transgenic | NF-kappa B - metabolism | Ubiquitination - immunology | MAP Kinase Signaling System - immunology | Animals | B-Lymphocytes - immunology | Flow Cytometry | Models, Animal | Mice | Receptors, Tumor Necrosis Factor - immunology | Ubiquitin-Protein Ligases - genetics | Real-Time Polymerase Chain Reaction | B-Lymphocytes - metabolism | Multiprotein Complexes - immunology | Signal transduction | TNF inhibitors | Cellular biology | Immune system | Animal models | canonical NF-κB pathway
B cell | linear ubiquitin chain assembly complex | antibody response | canonical NF‐κB pathway | ERK | Canonical NF-κB pathway | Linear ubiquitin chain assembly complex | Antibody response | ACTIVATION | COMPLEX | INDEPENDENT TYPE-2 ANTIGENS | BIOCHEMISTRY & MOLECULAR BIOLOGY | canonical NF-kappa B pathway | RECEPTOR | CELL BIOLOGY | CHRONIC PROLIFERATIVE DERMATITIS | LYMPHOCYTE DEVELOPMENT | SIGNALING PATHWAY | CHAINS | NF-KAPPA-B | NEMO | Immunity, Cellular - genetics | Electrophoresis, Polyacrylamide Gel | Mice, Inbred C57BL | NF-kappa B - immunology | Immunoblotting | Mice, Transgenic | NF-kappa B - metabolism | Ubiquitination - immunology | MAP Kinase Signaling System - immunology | Animals | B-Lymphocytes - immunology | Flow Cytometry | Models, Animal | Mice | Receptors, Tumor Necrosis Factor - immunology | Ubiquitin-Protein Ligases - genetics | Real-Time Polymerase Chain Reaction | B-Lymphocytes - metabolism | Multiprotein Complexes - immunology | Signal transduction | TNF inhibitors | Cellular biology | Immune system | Animal models | canonical NF-κB pathway
Journal Article
Nature Communications, ISSN 2041-1723, 04/2015, Volume 6, Issue 1, p. 6838
Histone deacetylase inhibitors (HDACi) are approved for treating certain haematological malignancies, however, recent evidence also illustrates they are...
MULTIPLE-MYELOMA | BURKITT-LYMPHOMA | ANTICANCER ACTIVITIES | EPIGENETIC CONTROL | MULTIDISCIPLINARY SCIENCES | GERMINAL CENTER | PROLIFERATIVE LUPUS NEPHRITIS | AUTOIMMUNE-DISEASE | LYN-DEFICIENT MICE | PRIMARY IMMUNE-RESPONSE | THERAPEUTIC ACTIVITIES | Cell Survival - drug effects | Mice, Inbred C57BL | Cells, Cultured | Male | Germinal Center - drug effects | Immunologic Memory - drug effects | B-Lymphocytes - drug effects | Animals | Cell Differentiation - drug effects | Lupus Erythematosus, Systemic - drug therapy | Female | Histone Deacetylase Inhibitors - pharmacology | Hydroxamic Acids - therapeutic use | Indoles - pharmacology | Indoles - therapeutic use | Cell Proliferation - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Drug Evaluation, Preclinical | Hydroxamic Acids - pharmacology
MULTIPLE-MYELOMA | BURKITT-LYMPHOMA | ANTICANCER ACTIVITIES | EPIGENETIC CONTROL | MULTIDISCIPLINARY SCIENCES | GERMINAL CENTER | PROLIFERATIVE LUPUS NEPHRITIS | AUTOIMMUNE-DISEASE | LYN-DEFICIENT MICE | PRIMARY IMMUNE-RESPONSE | THERAPEUTIC ACTIVITIES | Cell Survival - drug effects | Mice, Inbred C57BL | Cells, Cultured | Male | Germinal Center - drug effects | Immunologic Memory - drug effects | B-Lymphocytes - drug effects | Animals | Cell Differentiation - drug effects | Lupus Erythematosus, Systemic - drug therapy | Female | Histone Deacetylase Inhibitors - pharmacology | Hydroxamic Acids - therapeutic use | Indoles - pharmacology | Indoles - therapeutic use | Cell Proliferation - drug effects | Histone Deacetylase Inhibitors - therapeutic use | Drug Evaluation, Preclinical | Hydroxamic Acids - pharmacology
Journal Article
European Journal of Immunology, ISSN 0014-2980, 05/2014, Volume 44, Issue 5, pp. 1541 - 1551
IL‐12 is a heterodimeric cytokine composed of an α‐chain (p35) and a β‐chain (p40). Primarily produced by APCs, IL‐12 induces IFN‐γ production in T, B and NK...
Infection | IL‐12 | Bioactivity | Th1 immune responses | Rainbow trout | IL-12 | RAINBOW-TROUT | IFN-GAMMA | PROLIFERATIVE-KIDNEY-DISEASE | FUNCTIONAL-CHARACTERIZATION | IMMUNOLOGY | ADAPTIVE IMMUNITY | REGULATORY MECHANISMS | GENE-EXPRESSION | TELEOST FISH | CYTOKINE FAMILY | TROUT ONCORHYNCHUS-MYKISS | Oncorhynchus mykiss - metabolism | Th1 Cells - pathology | Fish Proteins - biosynthesis | Fish Proteins - immunology | Gene Expression Regulation - immunology | Male | Th1 Cells - immunology | Fish Diseases - pathology | Th1 Cells - metabolism | Animals | Interleukin-12 Subunit p35 - immunology | Interferon-gamma - immunology | Interleukin-12 Subunit p35 - biosynthesis | Fish Diseases - immunology | Female | Interleukin-12 Subunit p40 - immunology | Oncorhynchus mykiss - immunology | Immunity, Cellular | Interleukin-12 Subunit p40 - biosynthesis | Interferon-gamma - biosynthesis | Fish Diseases - metabolism | Immune response | Gene expression | Trout | Analysis | Fishes | Pathogens
Infection | IL‐12 | Bioactivity | Th1 immune responses | Rainbow trout | IL-12 | RAINBOW-TROUT | IFN-GAMMA | PROLIFERATIVE-KIDNEY-DISEASE | FUNCTIONAL-CHARACTERIZATION | IMMUNOLOGY | ADAPTIVE IMMUNITY | REGULATORY MECHANISMS | GENE-EXPRESSION | TELEOST FISH | CYTOKINE FAMILY | TROUT ONCORHYNCHUS-MYKISS | Oncorhynchus mykiss - metabolism | Th1 Cells - pathology | Fish Proteins - biosynthesis | Fish Proteins - immunology | Gene Expression Regulation - immunology | Male | Th1 Cells - immunology | Fish Diseases - pathology | Th1 Cells - metabolism | Animals | Interleukin-12 Subunit p35 - immunology | Interferon-gamma - immunology | Interleukin-12 Subunit p35 - biosynthesis | Fish Diseases - immunology | Female | Interleukin-12 Subunit p40 - immunology | Oncorhynchus mykiss - immunology | Immunity, Cellular | Interleukin-12 Subunit p40 - biosynthesis | Interferon-gamma - biosynthesis | Fish Diseases - metabolism | Immune response | Gene expression | Trout | Analysis | Fishes | Pathogens
Journal Article
British Journal of Ophthalmology, ISSN 0007-1161, 05/2015, Volume 99, Issue 5, pp. 700 - 704
Background/aims Tumour necrosis factor-α (TNF-α) is a key mediator of ocular inflammation and its interaction with the retinal pigment epithelium (RPE) may be...
GENE-EXPRESSION | OPHTHALMOLOGY | NEOVASCULARIZATION | BARRIER | Cell Line | Retinal Pigment Epithelium - metabolism | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Gene Expression Regulation - physiology | Gene Expression Profiling | Transcription Factors - genetics | Blotting, Western | HT29 Cells | Tumor Necrosis Factor-alpha - pharmacology | Real-Time Polymerase Chain Reaction | Retinal Pigment Epithelium - drug effects | Macular degeneration | Diabetic retinopathy | Tumor necrosis factor | Research | Gene expression | Risk factors | Proliferative vitreoretinopathy
GENE-EXPRESSION | OPHTHALMOLOGY | NEOVASCULARIZATION | BARRIER | Cell Line | Retinal Pigment Epithelium - metabolism | Epithelial Cells - metabolism | Epithelial Cells - drug effects | Humans | Gene Expression Regulation - physiology | Gene Expression Profiling | Transcription Factors - genetics | Blotting, Western | HT29 Cells | Tumor Necrosis Factor-alpha - pharmacology | Real-Time Polymerase Chain Reaction | Retinal Pigment Epithelium - drug effects | Macular degeneration | Diabetic retinopathy | Tumor necrosis factor | Research | Gene expression | Risk factors | Proliferative vitreoretinopathy
Journal Article
The Journal of Infectious Diseases, ISSN 0022-1899, 12/2007, Volume 196, Issue 11, pp. 1620 - 1628
We describe 2 spatially distinct foci of human African trypansomiasis in eastern Uganda. The Tororo and Soroti foci of Trypanosoma brucei rhodesiense infection...
Cytokines | Parasitic diseases | Virulence | Medical genetics | Infections | Glasgow coma scale | Parasites | Genotypes | Trypanosome | Blood plasma | INFECTIOUS DISEASES | INFECTIONS | CELL PROLIFERATIVE RESPONSES | NITRIC-OXIDE | RESISTANCE | SLEEPING SICKNESS | CNS | MICROBIOLOGY | IMMUNOLOGY | BRUCEI-BRUCEI | SUPPRESSION | IL-10 | Humans | Host-Parasite Interactions - genetics | Virulence - genetics | Glasgow Coma Scale | Polymerase Chain Reaction | Trypanosoma brucei rhodesiense - genetics | Blood-Brain Barrier - parasitology | Severity of Illness Index | Blood-Brain Barrier - immunology | Interferon-gamma - cerebrospinal fluid | Interleukins - blood | Malaria, Cerebral - parasitology | Antiviral Agents - blood | Malaria, Cerebral - immunology | Genotype | Host-Parasite Interactions - immunology | Coma - parasitology | Coma - immunology | Disease Progression | Trypanosomiasis, African - immunology | Phenotype | Animals | Trypanosoma brucei rhodesiense - pathogenicity | Uganda | Interferon-gamma - blood | virulence | interferon-gamma | African trypanosomiasis
Cytokines | Parasitic diseases | Virulence | Medical genetics | Infections | Glasgow coma scale | Parasites | Genotypes | Trypanosome | Blood plasma | INFECTIOUS DISEASES | INFECTIONS | CELL PROLIFERATIVE RESPONSES | NITRIC-OXIDE | RESISTANCE | SLEEPING SICKNESS | CNS | MICROBIOLOGY | IMMUNOLOGY | BRUCEI-BRUCEI | SUPPRESSION | IL-10 | Humans | Host-Parasite Interactions - genetics | Virulence - genetics | Glasgow Coma Scale | Polymerase Chain Reaction | Trypanosoma brucei rhodesiense - genetics | Blood-Brain Barrier - parasitology | Severity of Illness Index | Blood-Brain Barrier - immunology | Interferon-gamma - cerebrospinal fluid | Interleukins - blood | Malaria, Cerebral - parasitology | Antiviral Agents - blood | Malaria, Cerebral - immunology | Genotype | Host-Parasite Interactions - immunology | Coma - parasitology | Coma - immunology | Disease Progression | Trypanosomiasis, African - immunology | Phenotype | Animals | Trypanosoma brucei rhodesiense - pathogenicity | Uganda | Interferon-gamma - blood | virulence | interferon-gamma | African trypanosomiasis
Journal Article
Endocrine Journal, ISSN 0918-8959, 2012, Volume 59, Issue 8, pp. 641 - 652
The NF-κB pathway is a central signaling pathway for inflammatory and immune responses, and aberrant NF-κB signaling is implicated multiple disorders, such as...
Ubiquitin | NF-κB | Inflammation | Immunity | PROTEIN-KINASE-C | ACTIVATION | GENOTOXIC STRESS | CHAIN ASSEMBLY COMPLEX | RIG-I | NF-kappa B | CHRONIC PROLIFERATIVE DERMATITIS | SHARPIN | INTERACTING PROTEIN | ENDOCRINOLOGY & METABOLISM | DEGRADATION | POLYUBIQUITIN CHAINS | Polyubiquitin - metabolism | Osteogenesis - physiology | Neoplasms - etiology | Polyubiquitin - biosynthesis | Apoptosis - drug effects | Humans | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | NF-kappa B - metabolism | Inflammation - etiology | Ubiquitination | Animals | CD40 Antigens - metabolism | Carrier Proteins - metabolism | Immunity, Innate - physiology | Mice | Transcription Factors | Ubiquitins - metabolism
Ubiquitin | NF-κB | Inflammation | Immunity | PROTEIN-KINASE-C | ACTIVATION | GENOTOXIC STRESS | CHAIN ASSEMBLY COMPLEX | RIG-I | NF-kappa B | CHRONIC PROLIFERATIVE DERMATITIS | SHARPIN | INTERACTING PROTEIN | ENDOCRINOLOGY & METABOLISM | DEGRADATION | POLYUBIQUITIN CHAINS | Polyubiquitin - metabolism | Osteogenesis - physiology | Neoplasms - etiology | Polyubiquitin - biosynthesis | Apoptosis - drug effects | Humans | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - metabolism | Models, Molecular | NF-kappa B - metabolism | Inflammation - etiology | Ubiquitination | Animals | CD40 Antigens - metabolism | Carrier Proteins - metabolism | Immunity, Innate - physiology | Mice | Transcription Factors | Ubiquitins - metabolism
Journal Article
Molecular Carcinogenesis, ISSN 0899-1987, 05/2016, Volume 55, Issue 5, pp. 486 - 498
The tumor suppressive microRNA miR‐34a is transcriptionally regulated by p53 and shown to inhibit breast cancer cell proliferation as well as being a marker of...
artemisinin | Indole‐3‐carbinol | anti‐proliferative response | artesunate | CDK4 | Indole-3-carbinol | Anti-proliferative response | Artesunate | Artemisinin | BIOCHEMISTRY & MOLECULAR BIOLOGY | anti-proliferative response | CYCLE ARREST | KAPPA-B | P53 | ANTICANCER ACTIVITY | MESSENGER-RNAS | IN-VITRO | ONCOLOGY | UP-REGULATION | EXPRESSION | Cyclin-Dependent Kinase 4 - genetics | Humans | Cyclin-Dependent Kinase 4 - metabolism | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Artemisinins - pharmacology | Breast Neoplasms - genetics | MCF-7 Cells | Cell Line, Tumor | Female | Indoles - pharmacology | Cell Proliferation - drug effects | MicroRNAs - genetics | Gene Expression Regulation, Neoplastic - drug effects | Antineoplastic Agents, Phytogenic - pharmacology | Breast cancer | MicroRNA | Tumor proteins | Cancer cells | Genetic markers | Phytochemicals | Cancer therapies | MicroRNAs | Flow cytometry | p53 Protein | Gene expression | Ribonucleic acid--RNA | Ablation | Signal transduction | 3' Untranslated regions | Cell cycle | Breast | Tumor suppressor genes | Human behavior | Binding sites | Cancer | Tumors
artemisinin | Indole‐3‐carbinol | anti‐proliferative response | artesunate | CDK4 | Indole-3-carbinol | Anti-proliferative response | Artesunate | Artemisinin | BIOCHEMISTRY & MOLECULAR BIOLOGY | anti-proliferative response | CYCLE ARREST | KAPPA-B | P53 | ANTICANCER ACTIVITY | MESSENGER-RNAS | IN-VITRO | ONCOLOGY | UP-REGULATION | EXPRESSION | Cyclin-Dependent Kinase 4 - genetics | Humans | Cyclin-Dependent Kinase 4 - metabolism | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Dose-Response Relationship, Drug | Artemisinins - pharmacology | Breast Neoplasms - genetics | MCF-7 Cells | Cell Line, Tumor | Female | Indoles - pharmacology | Cell Proliferation - drug effects | MicroRNAs - genetics | Gene Expression Regulation, Neoplastic - drug effects | Antineoplastic Agents, Phytogenic - pharmacology | Breast cancer | MicroRNA | Tumor proteins | Cancer cells | Genetic markers | Phytochemicals | Cancer therapies | MicroRNAs | Flow cytometry | p53 Protein | Gene expression | Ribonucleic acid--RNA | Ablation | Signal transduction | 3' Untranslated regions | Cell cycle | Breast | Tumor suppressor genes | Human behavior | Binding sites | Cancer | Tumors
Journal Article
British Journal of Haematology, ISSN 0007-1048, 03/2016, Volume 172, Issue 6, pp. 889 - 901
Summary Pomalidomide is an IMiD® immunomodulatory agent, which has shown clinically significant benefits in relapsed and/or refractory multiple myeloma (rrMM)...
dexamethasone | apoptosis | myeloma | anti‐proliferative | pomalidomide | resistance | Resistance | Pomalidomide | Anti-proliferative | Dexamethasone | Myeloma | Apoptosis | SURVIVAL | CELLS | BIM | THALIDOMIDE | CEREBLON EXPRESSION | anti-proliferative | GLUCOCORTICOID-RECEPTOR | THERAPY | PLUS DEXAMETHASONE | HEMATOLOGY | LOW-DOSE DEXAMETHASONE | Immunomodulation - drug effects | Dexamethasone - administration & dosage | Apoptosis - drug effects | Humans | Drug Resistance, Neoplasm | Multiple Myeloma - immunology | Thalidomide - administration & dosage | Mice, SCID | Xenograft Model Antitumor Assays - methods | Drug Synergism | Thalidomide - analogs & derivatives | Multiple Myeloma - drug therapy | Multiple Myeloma - pathology | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Female | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Thalidomide - therapeutic use | Tumor Cells, Cultured | Multiple Myeloma - genetics | Multiple myeloma | Models | Interferon | Biological response modifiers | Gene expression | Steroids
dexamethasone | apoptosis | myeloma | anti‐proliferative | pomalidomide | resistance | Resistance | Pomalidomide | Anti-proliferative | Dexamethasone | Myeloma | Apoptosis | SURVIVAL | CELLS | BIM | THALIDOMIDE | CEREBLON EXPRESSION | anti-proliferative | GLUCOCORTICOID-RECEPTOR | THERAPY | PLUS DEXAMETHASONE | HEMATOLOGY | LOW-DOSE DEXAMETHASONE | Immunomodulation - drug effects | Dexamethasone - administration & dosage | Apoptosis - drug effects | Humans | Drug Resistance, Neoplasm | Multiple Myeloma - immunology | Thalidomide - administration & dosage | Mice, SCID | Xenograft Model Antitumor Assays - methods | Drug Synergism | Thalidomide - analogs & derivatives | Multiple Myeloma - drug therapy | Multiple Myeloma - pathology | Animals | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Female | Cell Proliferation - drug effects | Gene Expression Regulation, Neoplastic - drug effects | Thalidomide - therapeutic use | Tumor Cells, Cultured | Multiple Myeloma - genetics | Multiple myeloma | Models | Interferon | Biological response modifiers | Gene expression | Steroids
Journal Article