The pathogenicity of Th17 cells in autoimmune diseases.
Animals
Autoimmune Diseases
/ diagnosis
Autoimmunity
Cell Differentiation
/ immunology
Cytokines
/ metabolism
Disease Susceptibility
Environmental Exposure
Gastrointestinal Microbiome
Gene Expression Regulation
Humans
Inflammation Mediators
/ metabolism
Interleukin-17
/ biosynthesis
Lymphocyte Activation
/ immunology
Phenotype
Signal Transduction
T-Lymphocyte Subsets
/ cytology
Th17 Cells
/ cytology
Autoimmune arthritis
EAE
GM-CSF
IL-17
Rheumatoid arthritis
Th17 cells
Journal
Seminars in immunopathology
ISSN: 1863-2300
Titre abrégé: Semin Immunopathol
Pays: Germany
ID NLM: 101308769
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
received:
30
01
2019
accepted:
05
03
2019
pubmed:
21
3
2019
medline:
2
4
2020
entrez:
21
3
2019
Statut:
ppublish
Résumé
IL-17-producing T helper (Th17) cells have been implicated in the pathogenesis of many inflammatory and autoimmune diseases. Targeting the effector cytokines IL-17 and GM-CSF secreted by autoimmune Th17 cells has been shown to be effective for the treatment of the diseases. Understanding a molecular basis of Th17 differentiation and effector functions is therefore critical for the regulation of the pathogenicity of tissue Th17 cells in chronic inflammation. Here, we discuss the roles of proinflammatory cytokines and environmental stimuli in the control of Th17 differentiation and chronic tissue inflammation by pathogenic Th17 cells in humans and in mouse models of autoimmune diseases. We also highlight recent advances in the regulation of pathogenic Th17 cells by gut microbiota and immunometabolism in autoimmune arthritis.
Identifiants
pubmed: 30891627
doi: 10.1007/s00281-019-00733-8
pii: 10.1007/s00281-019-00733-8
doi:
Substances chimiques
Cytokines
0
IL17A protein, human
0
Inflammation Mediators
0
Interleukin-17
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
283-297Commentaires et corrections
Type : ErratumIn
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