IL-23 Activated γδ T Cells Affect Th17 Cells and Regulatory T Cells by Secreting IL-21 in Children with Primary Nephrotic Syndrome.
Scand J Immunol
; 87(1): 36-45, 2018 Jan.
Article
em En
| MEDLINE
| ID: mdl-29119640
ABSTRACT
This study (1) analysed the percentage of γδ T cells, γδ T cell subsets, Th17 cells and regulatory T cells (Treg cells) and (2) determined the role of IL-23 in primary nephrotic syndrome (PNS) patients with active disease and in remission. Eighty-four patients with PNS and 51 healthy age-matched controls were included in this study. The percentage of γδ T cells, γδ T cell subsets, Th17 cells and Treg cells in peripheral blood mononuclear cells (PBMCs) were analysed by fluorescence-activated cell sorting. PMBCs from PNS patients with active disease were cultured in the presence of IL-23, IL-23 and an IL-23 antagonist, or IL23 and an anti-IL-21 monoclonal antibody (mAb). The percentage of γδ T cells, IL-23R+ γδ T cells and IL-17+ γδ T cells were significantly increased in PNS patients with active disease. There was a positive correlation between the percentage of γδ T cells, IL-23R+ γδ T cells, IL-17+ γδ T cells and the Th17/Treg ratio. IL-23 increased the percentage of γδ T cells and Th17 cells and decreased the percentage of Treg cells in PBMCs isolated from PNS patients with active disease. Anti-IL-21 mAb reduced the percentage of γδ T cells and Th17 cells, but increased the percentage of Treg cells. γδ T cells, IL-17+ γδ T cells and IL-23R+ γδ T cells may be involved in the pathogenesis of paediatric PNS by modulating the balance of Th17/Treg cells. γδ T cells may cause an imbalance in Th17/Treg cells by secreting IL-21 in the presence of IL-23.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Ativação Linfocitária
/
Interleucinas
/
Receptores de Antígenos de Linfócitos T gama-delta
/
Linfócitos T Reguladores
/
Interleucina-23
/
Células Th17
/
Síndrome Nefrótica
Tipo de estudo:
Etiology_studies
Limite:
Adolescent
/
Child
/
Child, preschool
/
Female
/
Humans
/
Infant
/
Male
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article