Background: Autoimmune thyroiditis (AITD) is an organ-specific autoimmune disease. Substantial evidence suggests that Vitamin D (VitD) deficiency is closely associated with an increased risk of AITD. However, the effects of VitD3 on immune cells, especially Th17/Treg cell subsets, and the underlying molecular mechanism in AITD have not yet been investigated.
Methods: An experimental autoimmune thyroiditis (EAT) mouse model was established with a high-iodine diet. After 8 weeks, thyroid injury was assessed using hematoxylin and eosin (H&E) staining. ELISA was employed to measure serum levels of thyroxine (T3 and T4), thyroid autoimmune antibodies (Tg-Ab and TPO-Ab), and inflammatory cytokines. Flow cytometry and multiplex fluorescence immunohistochemical (mIHC) assays were used to analyze Th17/Treg cell subsets. The CCK-8 and flow cytometry assays were used to determine cell viability and apoptosis.
Results: Administration of VitD3 reduced thyroid follicle destruction, decreased lymphocyte infiltration, and lowered T3, T4, Tg-Ab, and TPO-Ab serum levels in EAT mice. VitD3 treatment also reduced the frequency of Th17 cells while promoting the Treg cell subset both in the thyroid tissue and in the splenocytes cultured in vitro. Furthermore, VitD3 administration suppressed the production of inflammatory cytokines in EAT mice. VitD3 was also found to regulate Treg cells' differentiation, viability, and apoptosis. Mechanistically, we discovered that VitD3 treatment upregulated YAP expression and activated the JAK/STAT pathway. Rescue assays confirmed that depletion of YAP counteracted the effects of VitD3 on Treg cell differentiation and function.
Conclusion: Vitamin D3 attenuates AITD by modulating Th17/Treg cell balance via regulating the YAP/JAK1/STAT1 axis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.imlet.2024.106890 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Association of anti-phosphatidylserine/prothrombin antibodies with adverse in vitro fertilization outcomes.
J Reprod Immunol
January 2025
Reproductive and Genetic Center, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230026, China. Electronic address:
Anti-phosphatidylserine/prothrombin antibodies (aPS/PT) are classified as non-criteria antiphospholipid antibodies (aPL), and are strongly associated with thrombosis and pregnancy complications linked to antiphospholipid syndrome (APS). This study aimed to investigate whether aPS/PT positivity is associated with adverse outcomes in vitro fertilization (IVF). The study included infertile women who tested positive aPS/PT and underwent IVF cycles, as well as infertile controls with pure tubal etiology.
View Article and Find Full Text PDFWKB ameliorates DSS-induced colitis through inhibiting enteric glial cells activation and altering the intestinal microbiota.
J Transl Med
January 2025
Department of Gastroenterology, Air Force Medical Center, No. 30 Fucheng Road, Haidian District, Beijing, 100142, China.
Background: Inflammatory bowel disease (IBD) is a chronic condition influenced by diet, which affects gut microbiota and immune functions. The rising prevalence of IBD, linked to Western diets in developing countries, highlights the need for dietary interventions. This study aimed to assess the impact of white kidney beans (WKB) on gut inflammation and microbiota changes, focusing on their effects on enteric glial cells (EGCs) and immune activity in colitis.
View Article and Find Full Text PDFDual neutralization of TGF-β and IL-21 regulates Th17/Treg balance by suppressing inflammatory signalling in the splenic lymphocytes of Staphylococcus aureus infection-induced septic arthritic mice.
Immunol Res
January 2025
Immunology Laboratory, Department of Physiology, University Colleges of Science and Technology, University of Calcutta, 92 APC Road, Calcutta, 700009, West Bengal, India.
Septic arthritis (SA) caused by Staphylococcus aureus is a severe inflammatory joint disease, characterized by synovitis accompanied with cartilage destruction and bone erosion. The available antibiotic treatment alone is insufficient to resolve the inflammation that leads to high rates of morbidity and mortality. Among the CD4 T helper lymphocytes, the Th17 and Tregs are key regulators of immune homeostasis.
View Article and Find Full Text PDFAg85B-Induced M1 Macrophage Polarization via the TLR4/TRAF6/NF-κB Axis Leading to Bronchial Epithelial Cell Damage and TH17/Treg Imbalance.
Curr Mol Med
January 2025
Endoscopy Center, Hunan Chest Hospital, Changsha, 410016, China.
Background: Antigen 85B (Ag85B) is a signature antigen of Mycobacterium tuberculosis (MTB). In this study, we aimed to investigate the impact of macrophages stimulated with Ag85B on bronchial epithelial cells and T cells, as well as the underlying mechanisms involved.
Methods: We used Ag85B to stimulate macrophage and investigated the impact of Ag85B on macrophage polarization.
MiR-519d-3p from Placenta-Derived Exosomes Induce Immune Intolerance Regulating Immune Cells, Contributing to the Pathogenesis of Preeclampsia.
Immunol Invest
January 2025
Department of Obstetrics and Gynecology, Medical Centre of Maternity and Child Health, Shengli Clinical Medical College of Fujian Medical University, Fujian, China.
Background: MiR-519d-3p, also called specific placenta biomarkers, is a member of the Chromosome 19 miRNA Cluster (C19MC) with the highest concentrations of miRNAs in human placenta and maternal serum. These miRNAs are secreted by fetal trophoblast cells within extracellular vesicles (EVs) and interact with the mother's immune cells, which has been proposed to be crucial for immunological tolerance at the placental-maternal interface. A key mechanism in preeclampsia, a multifactorial, multipath hypertensive pregnancy illness, is an immunological imbalance between the mother and the fetus.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!