Transcriptomic age acceleration is associated with plasmablast-related immune remodeling in IgG4-related disease

Clicks: 9
ID: 337812
2026
Free PDF
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.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #42 of 46 articles by views in Clinical & Experimental Immunology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create 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
Sign in to mint
Abstract
Abstract Biological aging profoundly influences immune function, yet its role in shaping immune remodeling within chronically inflamed tissues remains unclear. We investigated whether transcriptomic age identifies a plasmablast-associated immune aging pattern in IgG4-related disease (IgG4-RD). To address this question, bulk RNA sequencing was performed on submandibular gland lesions from 49 patients with IgG4-RD and 3 controls. Transcriptomic age (tAge) was estimated using a transcriptome-based aging model, and age acceleration was calculated as the residual from chronological age. Associations between age acceleration, immune transcriptional modules, and clinical characteristics were evaluated using Spearman correlation analyses. Transcriptomic age correlated with chronological age (ρ = 0.473, P< 0.001), whereas age acceleration was associated with serum IgG4 concentrations (ρ = 0.446, P = 0.001). Among immune transcriptional modules, the plasmablast signature showed the strongest positive association with age acceleration (ρ = 0.312, nominal P = 0.029), although this association did not remain significant after correction for multiple comparisons (FDR-adjusted P = 0.304). Germinal center B-cell and activated B-cell programs showed inverse trends. The plasmablast module also correlated with serum IgG4 levels. Together, these exploratory findings suggest a coordinated pattern linking transcriptomic age acceleration, plasmablast enrichment, and enhanced IgG4 responses. Rather than establishing a mechanistic pathway, these findings identify a candidate plasmablast-associated immune aging pattern that warrants validation in independent cohorts.
Reference Key
openalex_W7224593196 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Motohisa Yamamoto, Ryuta Kamekura, Masaaki Uehara, Yuta Ichii, Kenichi Takano
Are you one of these authors? Claim your profile
Journal Clinical & Experimental Immunology
Year 2026
DOI
10.1093/cei/uxag069
URL
https://doi.org/10.1093/cei/uxag069
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.