ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Genetic mechanisms of pollinosis: interactions between genes and environmental factors.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Intragenic deletions from whole genome sequencing of 1054 suicide deaths.Research square · 2026Article
- The role of calcium homeostasis dysregulation in allergic rhinitis.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundPollinosis, or pollen-induced allergic rhinitis, results from complex interactions among genetic susceptibility, environmental exposures, and epigenetic regulation. Risk variants within Th2 signaling and IgE regulatory pathways (e.g., IL13, IL4R, ADAM33) have been identified, while genome-wide association and transcriptomic analyses implicate additional genes involved in immune regulation and epithelial barrier integrity. Environmental factors such as urbanization, pollen burden, and air pollution further amplify disease risk, partly through epigenetic modifications.
methodsThis narrative review synthesizes evidence from candidate-gene studies, genome-wide association studies (GWAS), transcriptomic datasets, and epigenetic investigations, with particular emphasis on gene-environment interactions in pollen-induced allergic rhinitis. We highlight replicated findings, compare results across study designs and populations, and critically appraise the strength of evidence and methodological limitations.
resultsConvergent data support the contribution of Th2-related and IgE-regulatory loci, alongside additional GWAS-implicated genes, to pollinosis susceptibility. Transcriptomic and epigenomic studies reveal dysregulated immune pathways and environmentally induced DNA methylation and chromatin changes. However, replication across ancestries is limited, variant-to-function mechanisms remain incompletely defined, and current polygenic risk scores explain only a modest proportion of disease variance. Integration of environmental metrics such as pollen load and air pollution into genetic and epigenetic models is still at an early stage.
conclusionsBridging molecular discoveries with environmental and clinical contexts is essential to advance precision prevention and personalized management of pollinosis. Future work should focus on fine-mapping with tissue-specific colocalization, seasonal single-cell multi-omics, and quantitative models that combine genetic risk with real-time exposure data. Clinically, polygenic risk stratification and individualized immunotherapy hold promise, but their predictive performance, feasibility, and cost-effectiveness require validation in large, ancestrally diverse cohorts.
Indexed as
Identifiers
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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.