Genetic mechanisms of pollinosis: interactions between genes and environmental factors.
Pollinosis, 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.
This 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.
Convergent 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.
Bridging 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.
This 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.
Convergent 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.
Bridging 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.