Enhancer of zeste homolog 2 regulates B-cell responses in a NOD.H-2h4 model of spontaneous autoimmune thyroiditis
Clicks: 6
ID: 327205
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This
article has not been analysed, so there is no overall score —
reader engagement is measured and shown alongside.
Reader Engagement
Emerging Content
1.5
/100
6 views
5 readers
AI Quality Assessment
Not analyzed
Readership in this journal
EmergingRanked #297 of 308 articles by views in american journal of physiology endocrinology and metabolism
Most read
Least read
Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 308 in total.
Mint this article as an NFT
Not yet mintedCreate a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.
5
SUSD
one-off · no wallet required
Abstract
BACKGROUND: Hashimoto's thyroiditis (HT) is a prevalent autoimmune thyroid disease characterized by lymphocytic infiltration and autoantibody production. Our previous findings showed that enhancer of zeste homolog 2 (EZH2) and the B cell-related transcription factor BACH2 are upregulated in HT thyroid tissues. However, the role of EZH2 in B cell-mediated autoimmunity remains unclear. OBJECTIVE: To investigate how EZH2 regulates B cell responses in a spontaneous autoimmune thyroiditis (SAT) mouse model, and to explore potential downstream epigenetic mechanisms, including BACH2. METHODS: A NOD.H-2h4 mouse model of SAT was used to assess the effect of the EZH2 catalytic activity inhibitor GSK126 on thyroid inflammation and B cell responses. The human B-lymphocyte cell line GM12878 underwent EZH2 knockdown or was treated with GSK126 to evaluate BACH2 expression, H3K27me3 levels, and IgG secretion. ChIP-qPCR and luciferase assays were employed to examine EZH2-dependent regulation of BACH2, and rescue experiments were conducted using BACH2 overexpression. RESULTS: In SAT mice, GSK126 reduced thyroid lymphocytic infiltration, decreased CD19+ and IgG+ B cell infiltration, and lowered thyroidal IgG and serum IgG levels. In vitro, pharmacological inhibition of EZH2 catalytic activity or knockdown suppressed BACH2, reduced H3K27me3, and diminished IgG secretion. Luciferase and ChIP-qPCR assays supported EZH2-dependent regulation of BACH2, and BACH2 overexpression partially restored BACH2 expression but did not fully rescue IgG production after EZH2 methyltransferase activity inhibition. CONCLUSION: EZH2 contributes to B cell-mediated immune responses and IgG production through epigenetic mechanisms in SAT. BACH2 may represent one downstream target of EZH2, but additional pathways are likely involved.
| Reference Key |
openalex_W7204852373
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | Shengguo Yi, Xinnan Li, Yedi Cao, Guizhi Lu, Jixin Zhang, Y Q Zhang, Nan Yu, Youyuan Huang, Chenxue Qu, Junqing Zhang, Ying Gao |
| Journal | american journal of physiology endocrinology and metabolism |
| Year | 2026 |
| DOI |
10.1210/endocr/bqag096
|
| URL | |
| Keywords | Keywords not found |
Citations
No citations found. To add a citation, contact the admin at info@scimatic.org
Comments
No comments yet. Be the first to comment on this article.