ArticleMolecular therapy. Nucleic acids2025
HLA-DQB1-mediated B cell-epithelial crosstalk drives EBV-associated inflammation in Hunner-type interstitial cystitis.
Article in Molecular therapy. Nucleic acids, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hunner-type interstitial cystitis (HIC) is a chronic condition marked by persistent pain and inflammation. To elucidate its immunogenetic drivers, we integrated bulk RNA sequencing and single-cell RNA sequencing datasets with targeted major histocompatibility complex (MHC) sequencing. Transcriptomic analysis revealed selective expansion of B cells and epithelial cells, with strong enrichment of Epstein-Barr virus (EBV) response signatures. CellChat and NicheNet modeling uncovered bidirectional communication wherein B cells secrete IL-1β, FGF2, LIF, and TNFSF9, activating prostaglandin synthesis, matrix metalloproteinases, and stress genes in epithelial cells. In turn, epithelial BMP4, TGF-β2, and SHH modulate B cell survival. SCENIC regulatory network analysis identified IRF8 as the top B cell regulator; its regulon controls HLA-DQB1, CD40, and CIITA, linking EBV latency to heightened antigen presentation. Among differentially expressed genes, HLA-DQB1 was the most strongly induced in EBV
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.