Molecular Mechanisms in Allergic Rhinitis

Allergic rhinitis arises from a type I hypersensitivity reaction in which environmental allergens breach the nasal epithelium and stimulate an immune cascade dominated by immunoglobulin E production. Sensitisation of mast cells and basophils through allergen-IgE cross-linking triggers mediator release, leading to sneezing, nasal obstruction and pruritus. Dendritic cells orchestrate T-cell differentiation towards a Th2 phenotype under the influence of interleukins IL-4, IL-5 and IL-13, reinforcing eosinophil activation and mucosal inflammation. Concurrently, epithelial cells contribute to barrier integrity and cytokine secretion, while innate pathways such as NF-κB signalling modulate inflammatory gene transcription. Emerging evidence emphasises the role of non-coding RNAs and epigenetic modifications in fine-tuning immune responses, with microRNAs, long non-coding RNAs and circular RNAs acting as essential regulators of cell differentiation, cytokine production and signal transduction. Dysregulation of JAK/STAT signalling and competing endogenous RNA networks has illuminated new therapeutic targets. Together, these molecular insights underpin novel diagnostic biomarkers and precision interventions aimed at restoring immune homeostasis and ameliorating symptoms.

Research from Nature Portfolio

Recent studies have revealed how a specific long non-coding RNA modulates epithelial cell fate and inflammatory signalling. One investigation demonstrated that silencing of a particular lncRNA alleviates allergic rhinitis symptoms by reducing epithelial cell apoptosis and downregulating JAK/STAT3 pathway activation through interaction with a FOSL2 transcription factor, thereby diminishing local cytokine release. In parallel, research into epithelial cell-derived microRNA has shown its capacity to induce IL-10-producing monocytes, which exert an immunosuppressive effect on effector T cells and curb Th2-driven inflammation, highlighting an endogenous mechanism of immune regulation within the nasal mucosa.

Molecular Mechanisms in Allergic Rhinitis publication trend

The graph below shows the total number of articles in molecular mechanisms in allergic rhinitis across all publications each year (not limited to Nature Index journals).

Technical terms

Long non-coding RNA (lncRNA): RNA transcripts longer than 200 nucleotides that regulate gene expression without encoding proteins.

MicroRNA (miRNA): Short RNA molecules (~22 nucleotides) that modulate gene expression post-transcriptionally by targeting messenger RNAs.

Th2 cells: A subset of CD4+ T helper cells that produce IL-4, IL-5 and IL-13, driving type 2 immune responses.

Competing endogenous RNA (ceRNA): RNA molecules that sequester miRNAs, thereby influencing the repression of other target transcripts.

JAK/STAT3 pathway: A signalling cascade where cytokine receptor activation leads to phosphorylation of JAK kinases and STAT3 transcription factor, regulating inflammatory gene expression.

References

1. MIR222HG attenuates macrophage M2 polarization and allergic inflammation in allergic rhinitis by targeting the miR146a-5p/TRAF6/NF-κB axis. Frontiers in Immunology (2023).
2. Genetics and Epigenetics in Allergic Rhinitis. Genes (2021).
3. Emerging role of non-coding RNAs in allergic disorders. Biomedicine & Pharmacotherapy (2020).
4. Epithelial cell-derived micro RNA-146a generates interleukin-10-producing monocytes to inhibit nasal allergy. Scientific Reports (2015).
5. LncRNA HCP5 Participates in the Tregs Functions in Allergic Rhinitis and Drives Airway Mucosal Inflammatory Response in the Nasal Epithelial Cells. Inflammation (2022).
6. Mechanism of TCONS_00147848 regulating apoptosis of nasal mucosa cells and alleviating allergic rhinitis through FOSL2-mediated JAK/STAT3 signaling pathway. Scientific Reports (2021).