miR-106b-5p induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura through NR4A3/Foxp3 pathway.
Animals
Base Sequence
Cell Differentiation
Child
Child, Preschool
DNA-Binding Proteins
/ metabolism
Female
Forkhead Transcription Factors
/ metabolism
Gene Silencing
Humans
Male
Mice, Inbred BALB C
MicroRNAs
/ blood
Platelet Count
Purpura, Thrombocytopenic, Idiopathic
/ blood
Receptors, Steroid
/ metabolism
Receptors, Thyroid Hormone
/ metabolism
Signal Transduction
T-Lymphocytes, Regulatory
/ immunology
Th17 Cells
/ immunology
NR4A3
immune imbalance
immune thrombocytopenic purpura
mir-106b-5p
Journal
Cell cycle (Georgetown, Tex.)
ISSN: 1551-4005
Titre abrégé: Cell Cycle
Pays: United States
ID NLM: 101137841
Informations de publication
Date de publication:
06 2020
06 2020
Historique:
pubmed:
24
4
2020
medline:
27
8
2021
entrez:
24
4
2020
Statut:
ppublish
Résumé
Immune imbalance of regulatory T cells (Treg)/T helper 17 cells (Th17) contributes to the development of immune thrombocytopenic purpura (ITP). The dysregulation of miRNAs is important in the development of ITP. However, the role of miR-106b-5p in Treg/Th17 imbalance remains unknown in ITP. Peripheral blood was collected from patients with ITP and healthy controls, and CD4 + T cells were further isolated. miR-106b-5p, nuclear receptor subfamily 4 group A member 3 (NR4A3), forkhead box protein 3 (Foxp3), IL-17A, and TGF-β expressions were detected by qRT-PCR, western blot, or ELISA. The effect of miR-106b-5p on NR4A3 was detected by dual-luciferase reporter gene assay. Compared with healthy controls, miR-106b-5p was elevated in peripheral blood of patients with ITP, and NR4A3 expression was decreased. sh-NR4A3 significantly decreased Foxp3 and TGF-β expressions, indicating that NR4A3 may regulate Treg differentiation via Foxp3. Additionally, NR4A3 was identified to be a target of miR-106b-5p, and miR-106b-5p was able to negatively modulate NR4A3 expression. Moreover, we found miR-106b-5p induced immune imbalance of Treg/Th17 through NR4A3. miR-106b-5p regulated immune imbalance of Treg/Th17 in ITP through the NR4A3/Foxp3 pathway.
Sections du résumé
BACKGROUND
Immune imbalance of regulatory T cells (Treg)/T helper 17 cells (Th17) contributes to the development of immune thrombocytopenic purpura (ITP). The dysregulation of miRNAs is important in the development of ITP. However, the role of miR-106b-5p in Treg/Th17 imbalance remains unknown in ITP.
MATERIALS AND METHODS
Peripheral blood was collected from patients with ITP and healthy controls, and CD4 + T cells were further isolated. miR-106b-5p, nuclear receptor subfamily 4 group A member 3 (NR4A3), forkhead box protein 3 (Foxp3), IL-17A, and TGF-β expressions were detected by qRT-PCR, western blot, or ELISA. The effect of miR-106b-5p on NR4A3 was detected by dual-luciferase reporter gene assay.
RESULTS
Compared with healthy controls, miR-106b-5p was elevated in peripheral blood of patients with ITP, and NR4A3 expression was decreased. sh-NR4A3 significantly decreased Foxp3 and TGF-β expressions, indicating that NR4A3 may regulate Treg differentiation via Foxp3. Additionally, NR4A3 was identified to be a target of miR-106b-5p, and miR-106b-5p was able to negatively modulate NR4A3 expression. Moreover, we found miR-106b-5p induced immune imbalance of Treg/Th17 through NR4A3.
CONCLUSION
miR-106b-5p regulated immune imbalance of Treg/Th17 in ITP through the NR4A3/Foxp3 pathway.
Identifiants
pubmed: 32323598
doi: 10.1080/15384101.2020.1746485
pmc: PMC7469554
doi:
Substances chimiques
DNA-Binding Proteins
0
FOXP3 protein, human
0
Forkhead Transcription Factors
0
MIRN106 microRNA, human
0
MicroRNAs
0
NR4A3 protein, human
0
Receptors, Steroid
0
Receptors, Thyroid Hormone
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1265-1274Commentaires et corrections
Type : ErratumIn
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