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interleukin-23 subunit p19 (38) 38
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interleukin-12 - immunology (36) 36
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interleukin-17 - antagonists & inhibitors (35) 35
treatment outcome (35) 35
dendritic cells - immunology (34) 34
interleukin-23 - genetics (34) 34
interleukin-23 subunit p19 - genetics (34) 34
interleukin-23 subunit p19 - immunology (34) 34
pathogenesis (34) 34
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lymphocytes (31) 31
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gene expression (30) 30
abridged index medicus (29) 29
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disease models, animal (29) 29
inflammatory bowel disease (29) 29
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Immunity, ISSN 1074-7613, 10/2015, Volume 43, Issue 4, pp. 739 - 750
Interleukin-23 (IL-23) and IL-17 are cytokines currently being targeted in clinical trials. Although inhibition of both of these cytokines is effective for... 
INFLAMMATORY-BOWEL-DISEASE | CHRONIC PLAQUE PSORIASIS | CROHNS-DISEASE | EPITHELIAL-CELLS | COLITIS | LIPOPOLYSACCHARIDE-BINDING PROTEIN | DOUBLE-BLIND | RECEPTOR COMPLEX | IMMUNOLOGY | T-CELLS | TH17 CELLS | T-Lymphocyte Subsets - immunology | Interleukin-23 Subunit p19 - antagonists & inhibitors | Intestinal Mucosa - physiopathology | ATP Binding Cassette Transporter, Sub-Family B - deficiency | Receptors, Interleukin-17 - immunology | Epithelium - physiopathology | Interleukin-17 - immunology | Interleukin-17 - physiology | Transcriptome | Helicobacter Infections - complications | Interleukin-12 Subunit p40 - antagonists & inhibitors | T-Lymphocytes, Regulatory - immunology | Receptors, Interleukin-17 - physiology | Female | Colitis - drug therapy | Colitis - immunology | Interleukin-23 - physiology | Disease Models, Animal | Gene Expression Regulation - immunology | Immunoglobulin G - therapeutic use | Helicobacter Infections - immunology | Receptors, Interleukin-17 - antagonists & inhibitors | Permeability | Disease Progression | Interleukin-23 - immunology | Mice, Knockout | Colitis - etiology | Animals | Colitis - microbiology | Forkhead Transcription Factors - analysis | Immunization, Passive | Mice | Interleukin-23 Subunit p19 - immunology | Colitis | Psoriasis | Interleukins | Drug resistance | Analysis | Mortality | Inflammatory bowel disease | Studies | Pathology | Flow cytometry | Immunoglobulins | Histopathology | Cytokines | Infections | Inflammation | Gene expression | Crohns disease
Journal Article
Lancet, The, ISSN 0140-6736, 2017, Volume 389, Issue 10080, pp. 1699 - 1709
Summary Background The interleukin-23 pathway is implicated genetically and biologically in the pathogenesis of Crohn's disease. We aimed to assess the... 
Internal Medicine | TRIAL | CELLS | MEDICINE, GENERAL & INTERNAL | ANTI-TNF | INFLAMMATORY-BOWEL-DISEASE | EFFICACY | ULCERATIVE-COLITIS | NECROSIS-FACTOR ANTAGONISTS | ANTITUMOR | MAINTENANCE THERAPY | FACTOR-ALPHA | Severity of Illness Index | Interleukin-23 Subunit p19 - antagonists & inhibitors | Double-Blind Method | Drug Administration Schedule | Humans | Middle Aged | Antibodies, Monoclonal - adverse effects | Gastrointestinal Agents - administration & dosage | Antibodies, Monoclonal - therapeutic use | Male | Treatment Outcome | Remission Induction | Dose-Response Relationship, Drug | Young Adult | Antibodies, Monoclonal - administration & dosage | Crohn Disease - drug therapy | Adolescent | Gastrointestinal Agents - therapeutic use | Adult | Female | Aged | Gastrointestinal Agents - adverse effects | Clinical trials | Monoclonal antibodies | Medicine, Experimental | Medical research | Interleukins | Intravenous administration | Pathogenesis | Mucosa | Interleukin | Interleukin 23 | Antagonists | Intravenous therapy | Randomization | Endoscopes | Motivation | Gastroenterology | Remission | Tumor necrosis factor-TNF | Colon | Safety | Active control | Chronic illnesses | Psoriasis | Cytokines | Ileitis | Nausea | Inflammation | Crohn's disease | Disease control | Patients | Ileum | Crohns disease | Inflammatory bowel disease | Interactive systems | Tumor necrosis factor | Ulcers | TNF inhibitors | Tumors
Journal Article
Journal of Immunology, ISSN 0022-1767, 10/2009, Volume 183, Issue 8, pp. 5418 - 5427
IFN-beta-1a has been used over the past 15 years as a primary therapy for relapsing-remitting multiple sclerosis (MS). However, the immunomodulatory mechanisms... 
EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | GROWTH-FACTOR-BETA | T(H)17 CELLS | MULTIPLE-SCLEROSIS | DENDRITIC CELLS | MESSENGER-RNA EXPRESSION | CENTRAL-NERVOUS-SYSTEM | INTERFERON-BETA | IMMUNOLOGY | UP-REGULATION | T-CELLS | Receptors, CCR6 - immunology | Interleukin-12 Subunit p35 - metabolism | Interleukin-23 Subunit p19 - antagonists & inhibitors | Dendritic Cells - immunology | Humans | Receptors, CCR6 - antagonists & inhibitors | CD4-Positive T-Lymphocytes - immunology | Receptors, Interleukin - metabolism | Interleukin-23 Subunit p19 - metabolism | STAT1 Transcription Factor - metabolism | Interleukin-1beta - metabolism | Receptors, Retinoic Acid - immunology | Phosphorylation - immunology | Phosphorylation - drug effects | Receptors, Thyroid Hormone - immunology | Interleukin-1beta - antagonists & inhibitors | Nuclear Receptor Subfamily 1, Group F, Member 3 | Receptors, Interleukin - immunology | Receptors, Interleukin - antagonists & inhibitors | Receptors, Retinoic Acid - metabolism | Cell Differentiation - immunology | Interferon beta-1a | Up-Regulation - immunology | Interleukin-23 Subunit p19 - immunology | STAT3 Transcription Factor - immunology | Interleukin-10 - immunology | Interleukin-17 - immunology | STAT1 Transcription Factor - drug effects | T-Lymphocytes, Helper-Inducer - drug effects | T-Lymphocytes, Helper-Inducer - immunology | Receptors, CCR6 - metabolism | Interleukin-10 - metabolism | Dendritic Cells - drug effects | Interleukin-10 - agonists | STAT3 Transcription Factor - metabolism | Cells, Cultured | Interleukin-1beta - immunology | Interleukin-12 Subunit p35 - agonists | Down-Regulation - drug effects | STAT1 Transcription Factor - immunology | Receptors, Thyroid Hormone - metabolism | Up-Regulation - drug effects | Interferon-beta - pharmacology | Interleukin-12 Subunit p35 - immunology | Cell Differentiation - drug effects | Down-Regulation - immunology | STAT3 Transcription Factor - drug effects | Multiple Sclerosis - immunology | CD4-Positive T-Lymphocytes - drug effects
Journal Article
Journal Article
Expert Opinion on Therapeutic Targets, ISSN 1472-8222, 05/2014, Volume 18, Issue 5, pp. 513 - 525
Journal Article
Journal of Immunology, ISSN 0022-1767, 01/2012, Volume 188, Issue 2, pp. 753 - 764
Journal Article
Diabetes, Obesity and Metabolism, ISSN 1462-8902, 08/2018, Volume 20, Issue 8, pp. 1859 - 1867
Aims Our current understanding of the pathogenesis of type 1 diabetes (T1D) arose, in large part, from studies using the non‐obese diabetic (NOD) mouse model.... 
type 1 diabetes | inflammatory pathways | human islets | short‐duration T1D | IL23 | T1D | functional genomics | IL23/p19 | RNA‐sequencing | RNA-sequencing | short-duration T1D | POPULATION | COMBINATION THERAPY | MOUSE | MELLITUS | PANCREATIC-ISLETS | MODELS | RNA-SEQ | ENDOCRINOLOGY & METABOLISM | p19 | INSULITIS | T-CELLS | Islets of Langerhans - drug effects | Interleukin-23 Subunit p19 - antagonists & inhibitors | Diabetes Mellitus, Type 1 - prevention & control | Humans | Diabetes Mellitus, Type 1 - metabolism | Antibodies, Monoclonal - therapeutic use | Male | Gene Expression Profiling | Interleukin-23 Subunit p19 - metabolism | Islets of Langerhans - metabolism | Interleukin-23 Subunit p19 - genetics | Adult | Female | Diabetes Mellitus, Type 1 - immunology | Child | Islets of Langerhans - pathology | Diabetes Mellitus, Type 1 - physiopathology | Gene Expression Regulation | Islets of Langerhans - immunology | Immunity, Innate | Disease Progression | Proof of Concept Study | Disease-Free Survival | Animals | Mice, Inbred NOD | Tissue Donors | Cadaver | Cluster Analysis | Genetic research | Gene expression | Type 1 diabetes | Genes | Analysis | Translation | Genomic analysis | Therapeutic applications | Diabetes mellitus | Data processing | Innate immunity | Diabetes mellitus (insulin dependent) | Inflammation | Ribonucleic acid--RNA | Rodents | Monoclonal antibodies | Diabetes | Pancreas
Journal Article
BioMetals, ISSN 0966-0844, 10/2015, Volume 28, Issue 5, pp. 891 - 902
Journal Article
Dermatologic Therapy, ISSN 1396-0296, 11/2017, Volume 30, Issue 6, pp. e12555 - n/a
The rapid progress of genetic engineering furthermore opens up new prospects in the therapy of this difficult‐to‐treat disease. IL‐23 inhibitors,... 
treatment | PDE4 inhibitors | psoriasis | therapy | biological drugs | immune‐modulating | IL‐23 inhibitors | JAK inhibitors | IL-23 inhibitors | immune-modulating | CONTROLLED-TRIAL | MODERATE | EFFICACY | SAFETY | PHASE-III | GUSELKUMAB | INTERLEUKIN-23 | DERMATOLOGY | APREMILAST | PLAQUE PSORIASIS | TILDRAKIZUMAB | Interleukin-23 Subunit p19 - antagonists & inhibitors | Humans | Psoriasis - diagnosis | Dermatologic Agents - therapeutic use | Janus Kinases - metabolism | Molecular Targeted Therapy | Dermatologic Agents - adverse effects | Interleukin-23 Subunit p19 - metabolism | Phosphodiesterase 4 Inhibitors - adverse effects | Cyclic Nucleotide Phosphodiesterases, Type 4 - metabolism | Skin - pathology | Skin - immunology | Psoriasis - immunology | Psoriasis - drug therapy | Phosphodiesterase 4 Inhibitors - therapeutic use | Treatment Outcome | Skin - enzymology | Janus Kinases - antagonists & inhibitors | Janus Kinase Inhibitors - adverse effects | Animals | Janus Kinase Inhibitors - therapeutic use | Signal Transduction - drug effects | Cyclic Nucleotide Phosphodiesterases, Type 4 - immunology | Interleukin-23 Subunit p19 - immunology | Psoriasis - enzymology | Skin - drug effects | Psoriasis | Interleukins | Dermatology | Formulae, receipts, prescriptions | Monoclonal antibodies | Mutual fund industry | Dermatologic agents | Genetic engineering | Drug therapy
Journal Article