Regulatory T cell features in chronic granulomatous disease.
Adolescent
Adult
Apoptosis
/ physiology
Autoimmunity
/ immunology
CD4 Lymphocyte Count
Child
Child, Preschool
Female
Granulomatous Disease, Chronic
/ immunology
Humans
Male
NADPH Oxidase 2
/ deficiency
NADPH Oxidases
/ deficiency
Neutrophils
/ immunology
Reactive Oxygen Species
/ metabolism
T-Lymphocytes, Regulatory
/ immunology
chronic granulomatous disease
inflammation
regulatory T cell
Journal
Clinical and experimental immunology
ISSN: 1365-2249
Titre abrégé: Clin Exp Immunol
Pays: England
ID NLM: 0057202
Informations de publication
Date de publication:
08 2019
08 2019
Historique:
accepted:
25
03
2019
pubmed:
30
3
2019
medline:
22
4
2020
entrez:
30
3
2019
Statut:
ppublish
Résumé
Chronic granulomatous disease (CGD) is a primary immunodeficiency caused by mutations in any of the genes encoding the phagocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system, responsible for the production of reactive oxygen species (ROS). CGD is marked by invasive bacterial and fungal infections and by autoinflammation/autoimmunity, of which the exact pathophysiology remains elusive. Contributing factors include decreased neutrophil apoptosis, impaired apoptotic neutrophil clearance, increased proinflammatory protein expression and reduced ROS-mediated inflammasome dampening. We have explored a fundamentally different potential mechanism: it has been reported that macrophage-mediated induction of regulatory T cells (T
Identifiants
pubmed: 30924925
doi: 10.1111/cei.13300
pmc: PMC6642867
doi:
Substances chimiques
Reactive Oxygen Species
0
CYBB protein, human
EC 1.6.3.-
NADPH Oxidase 2
EC 1.6.3.-
NADPH Oxidases
EC 1.6.3.-
neutrophil cytosolic factor 1
EC 1.6.3.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
222-229Informations de copyright
© 2019 British Society for Immunology.
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