ArticleCell communication and signaling : CCS2026
COVID-19 is associated with epigenetic dysregulation in regulatory B cells linked to recurrent pregnancy loss.
Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent pregnancy loss (RPL) affects 1-2% of reproductive-aged women, often with unexplained immune etiology. Regulatory B cells (Bregs) maintain maternal-fetal tolerance via interleukin-10 (IL-10) and are dysfunctional in RPL, but environmental triggers remain unknown. We aimed to determine whether SARS-CoV-2 infection is associated with persistent Breg dysfunction in RPL patients through epigenetic mechanisms and evaluate therapeutic rescue strategies. In this study, we analyzed peripheral blood from RPL patients (n = 30) and fertile controls (n = 30) with confirmed COVID-19 (2020-2022). Breg frequency (CD19⁺CD24hiCD38hi), IL-10 production, and epigenetic states (ATAC-seq, ChIP-qPCR, bisulfite sequencing) were assessed. RNA-seq defined transcriptional programs. Functional rescue was tested using HDACi/DNMTi in vitro and in a CBA/J × DBA/2J murine RPL model. The results showed that unlike fertile controls who recovered normal IL-10⁺ Breg function after COVID-19, RPL patients showed persistent IL-10 suppression associated with repressive chromatin, increased H3K27me3, decreased H3K27ac, and IL10 promoter hypermethylation. Non-infected RPL patients already had lower IL-10⁺ Breg frequencies; COVID-19 was associated with exacerbated IL-10 downregulation (ΔIL-10: 42.3% vs. 18.7%, p = 0.006). Epigenetic inhibition reversed this defect in vitro, and epigenetically reprogrammed Bregs improved pregnancy outcomes in mice (40% reduction in fetal resorption, p < 0.01). In conclusion, SARS-CoV-2 infection is associated with epigenetic silencing of IL10 in Bregs from RPL patients, linked to a durable tolerance defect. COVID-19 may represent a contributory environmental factor associated with RPL, and epigenetic modulation is a potential therapeutic avenue.
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.