Introduction: In recent decades, mast cells and their mediators have been increasingly recognized as central players in the pathogenesis of allergic rhinitis (AR), a complex chronic nasal disease characterized by pathological changes influenced by genetic factors, various immune cells, and environmental exposures. Mast cells are pivotal in allergic reactions, orchestrating inflammation and airway contraction through the secretion of diverse mediators. Prominent among these mediators are histamine and bioactive lipids, whose physiological effects are prominently observed during the acute phase of allergic reactions. The accumulation of mast cells in specific areas of allergic rhinitis may correlate with the disease’s phenotype, progression, and severity. In vivo experiments in mice have demonstrated that mast cells develop from mast cell progenitor cells, which are induced by inflammatory stimuli and subsequently migrate to the airway. Human mast cell progenitor cells have been identified in the bloodstream, with a high proportion potentially reflecting the persistent pathological changes associated with allergic rhinitis. The primary activation of mast cells in allergic rhinitis occurs via the cross-linking of IgE high-affinity receptors (Fcɛ RI) mediated by IgE in conjunction with allergens. However, mast cells can also be activated by a variety of other stimuli, including toll-like receptors and MAS-related G protein-coupled receptor X2. Rationale for this review: Despite the substantial progress in understanding the role of mast cells in allergic rhinitis, several critical gaps remain in our knowledge. The complex interplay between mast cells, their mediators, and the immune system in the context of AR is still not fully elucidated. Moreover, the specific mechanisms underlying the recruitment and activation of mast cell progenitor cells in the nasal mucosa remain poorly understood. Addressing these gaps is essential for developing more effective therapeutic strategies for allergic rhinitis. This review aims to provide a comprehensive and up-to-date synthesis of the current literature on the role and development of mast cells and their progenitor cells in allergic rhinitis, including the activation pathways implicated in the pathogenesis. Target audience: This review is intended for a broad audience, including researchers in the fields of immunology, allergy, and respiratory medicine, as well as clinicians who manage patients with allergic rhinitis. By summarizing the latest findings and highlighting the unresolved questions, this review aims to serve as a valuable reference for future research directions in mast cells and allergic rhinitis, ultimately contributing to improved patient care and outcomes.

To evaluate the correlation between glucosamine-6-phosphate isomerase 1 (GNPDA1) expression and prognosis, immune infiltration, and immune evasion in head and neck squamous cell carcinoma (HNSCC). We analyzed the expression of GNPDA1 in HNSCC tissues and obtained RNA sequence data from the Cancer Genome Atlas (TCGA) database. Kaplan–Meier survival analysis evaluated the relationship between GNPDA1 expression and advanced tumor stage, TNM stage, grading, and gender. Co-expressed genes with GNPDA1 were identified using TCGA data and annotated through gene ontology and Kyoto encyclopedia of genes and genomes analyses. A protein–protein interaction network was constructed using the STRING database. Single-sample gene set enrichment analysis was conducted based on TCGA and TIMER 2.0 databases to assess the correlation between GNPDA1 and immune infiltration. In addition, the location of GNPDA1 in tumor cell and immune cell structures was identified by the tumor immune stromal cells helper database, and potential protein-interacting molecules of GNPDA1 were elucidated in the STRING database. Potential GNPDA1 gene functions were assessed using gene set enrichment analysis. Our results indicate that the expression of GNPDA1 is elevated in HNSCC tissues (P < .05). GNPDA1 expression was positively correlated with tumor malignancy (P < .05) and negatively correlated with patient prognosis (P < .05). There was a significant correlation between high expression of GNPDA1 and advanced tumor stage, N-stage, or G-grade, and it was associated with gender. High GNPDA1 expression was associated with increased infiltration of resting CD4⁺T cells, macrophages M1 and M2, resting natural killer cells, monocytes, eosinophils, and naïve B cells (P < .05). In contrast, low GNPDA1 expression was associated with increased infiltration of activated natural killer cells, neutrophils, activated mast cells, macrophages M0, plasma cells, activated dendritic cells, CD8⁺T cells, memory B cells, regulatory T cells (Tregs), and naïve CD4⁺T cells (P < .05). In addition, GNPDA1 was observed to be closely associated with various immune evasion-related genes in HNSCC. The results of this study suggest that GNPDA1 can serve as a potential prognostic marker and therapeutic target for HNSCC and may be a key gene mediating immune evasion in HNSCC.

Di-O-benzoyldiethylene glycol, a novel eco-friendly plasticizer, lacks sufficient toxicological data, particularly regarding allergic rhinitis (AR). This study aims to elucidate its molecular mechanisms in AR induction and provide theoretical insights for targeted therapeutic strategies. Through network toxicology, molecular docking, and dynamics simulations, we retrieved Di-O-benzoyldiethylene glycol structures from PubChem, predicted its targets with multifaceted database analyses, and identified AR-related targets. Bioinformatics analysis highlighted immune and inflammatory pathways as key links and identified five core targets: AKT1, BCL2, EGFR, ESR1, and TNF. Molecular docking technology confirmed their strong binding affinity with AKT1, BCL2, EGFR, and ESR1.Molecular docking simulations indicate a high affinity binding between Di-O-benzoyldiethylene glycol and TNF, suggesting an effective interaction.In summary, Di-O-benzoyldiethylene glycol may promote the development of AR by regulating immune and inflammatory responses.These studies will provide important theoretical basis for preventing the progression of allergic diseases and evaluating the health risks of environmental pollution caused by new plasticizers.