IRAK2 emerges as candidate biomarker in allergic rhinitis study

Researchers report preliminary evidence that IRAK2, a gene known to regulate allergic airway inflammation, is significantly upregulated in the serum of patients with allergic rhinitis and may serve as a candidate diagnostic biomarker for the condition. The findings, published in BMC Immunology, also point to a possible pro-inflammatory role for IRAK2 in an in vitro model of nasal epithelial inflammation, although the authors stress that the mechanistic results are limited to the cell model and require in vivo validation.

Allergic rhinitis is a common chronic inflammatory condition of the nasal mucosa, and treatment options remain limited. According to the study’s background, IRAK2 had been implicated in allergic airway inflammation, but its expression, clinical value and mechanism in allergic rhinitis had not previously been explored, motivating the combined bioinformatics, clinical and laboratory approach.

The team first screened publicly available GEO datasets to identify differentially expressed genes and candidate genes related to allergic rhinitis. This bioinformatics analysis identified IRAK2 as a candidate gene in the disease, providing the starting point for clinical verification.

To test whether the candidate gene signal held up in patients, the investigators collected serum samples from 100 allergic rhinitis patients and 100 healthy controls. Serum IRAK2 levels were measured, and the researchers then performed correlation analysis, ROC curve analysis and logistic regression analysis on the resulting data.

The clinical results showed that serum IRAK2 was significantly upregulated in allergic rhinitis patients compared with healthy controls. In ROC curve analysis, IRAK2 showed favorable diagnostic accuracy for allergic rhinitis, and logistic regression indicated an independent statistical association with the disease.

Beyond the patient samples, the researchers used LPS-stimulated human nasal epithelial cells to explore what IRAK2 might be doing functionally. In this in vitro model, IRAK2 modulated the expression of NF-κB and p38 MAPK pathway-related proteins, accompanied by elevated inflammatory and oxidative stress levels as well as altered tight junction protein expression, which relates to epithelial barrier function.

The authors conclude that IRAK2 may function as a pro-inflammatory mediator in the LPS-induced cell model, driving inflammatory responses with involvement of the NF-κB and p38 MAPK pathways. They are explicit, however, that these mechanistic findings are limited to the cell model and require in vivo validation before any broader conclusions can be drawn.

On the diagnostic side, the study’s conclusion is similarly cautious: IRAK2 shows potential as a diagnostic biomarker for allergic rhinitis based on preliminary clinical evidence. The work is described as preliminary, and the article is being shared early as a peer-reviewed, accepted version that is subject to further edits before the final Version of Record.

For now, the study establishes the association in patient serum, the correlation with IgE and symptom scores, the diagnostic accuracy estimates, and the pathway-linked inflammatory effects observed in human nasal epithelial cells treated with LPS.

Subject of Research: The role of IRAK2 in allergic rhinitis as a diagnostic biomarker candidate and in vitro inflammatory mediator

Article Title: Preliminary evidence for IRAK2 as a potential biomarker and in vitro pro-inflammatory mediator in allergic rhinitis

Article References: Sun, H., & Li, R. (2026). Preliminary evidence for IRAK2 as a potential biomarker and in vitro pro-inflammatory mediator in allergic rhinitis. BMC Immunology. https://doi.org/10.1186/s12865-026-00926-5

Image Credits: AI Generated

DOI: 10.1186/s12865-026-00926-5

Keywords: allergic rhinitis, IRAK2, biomarker, NF-kB, p38 MAPK, serum diagnostics, nasal epithelial cells, inflammation, oxidative stress, total IgE, TNSS, GEO datasets