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Allergic rhinitis (AR) was first documented in traditional Chinese medicine in the “Yueling” chapter of the Chinese classic Liji for over 3000 years ago [1]. By contrast, the recognition of AR in Western medicine is more recent, beginning with John Bostock's first detailed clinical description of “hay fever” or “summer catarrh” in 1819 [2]. Despite this long history of awareness, AR became a public health burden particularly starting from the 1960s in parallel to industrialization and modernization reaching to pandemic numbers [3]. It is a major public health challenge in modern societies, imposing a significant economic burden and negatively affecting patients' quality of life, causing the highest numbers of absenteeism and presenteeism [4]. Recent epidemiological data from the Beijing Tongren Hospital based on three nationwide cross-sectional surveys has revealed a sharp rise in AR prevalence from 11.1% in 2005 to 17.2% in 2011, and further to 20.9% in 2019 in China, with Inner Mongolia now reaching 33.7% [5]. The rising public health threat of allergic diseases in China has made the official transition of anti-allergy efforts from individual responsibility to a public service guaranteed by the city. In the meanwhile, this intensified focus also led to sustained and substantial government investment and a substantial increase in research output from Chinese scholars during the past five years [6]. To this end, manuscript submissions by Chinese scholars to the journal Allergy rose sharply from 278 in 2023 to 311 in 2024, and further to 488 in 2025, positioning China as a major contributor. In terms of treating moderate-to-severe AR, a multicenter, randomized, double-blinded, placebo-controlled clinical trial have demonstrated that stapokibart (anti-IL-4R alpha chain monoclonal antibodies) administration in pollen season improved both nasal and ocular symptoms and quality of life in patients with moderate-to-severe seasonal AR [7]. This finding aligns with a network meta-analysis establishing that biologics, particularly anti-IL-4Rα therapy, are more effective in controlling nasal symptoms compared to either allergen immunotherapy or conventional pharmacotherapies [8]. Despite the limited global availability of biologics for seasonal AR, a multidisciplinary expert panel has been convened to standardize their use and promote evidence-based application in AR management [9]. The position paper defines indications for biologics in uncontrolled seasonal AR and recommends endotype-guided selection (e.g., elevated blood eosinophils) to optimize outcomes of biologics treatment [9]. Indeed, the position paper relies on highly controlled clinical trial data, which may not fully represent real-world practice. Therefore, additional real-world evidence is needed to address questions not adequately covered in trials. These include whether treatment can be safely extended to other indications [10], how to define a treatment response that accurately reflects meaningful improvements in patients' quality of life, and how to define the patterns and rationales for biologic switching in patients [11]. As a key contribution in the area of AR, the World Federation of Chinese Medicine Societies has published a guideline to support the evidence-informed integration of traditional Chinese medicine into AR management [12]. Together, these frameworks are designed to raise clinical benchmarks and advance more precise, standardized approaches to AR management, ultimately leading to a significant improvement in patients' quality of life. The increase in allergic airway diseases might be associated with average annual income, environmental factors, and vegetation coverage [5, 13, 14]. In response to this growing challenge, Chinese scholars have also characterized the national allergen profile [15, 16], which has been further confirmed by digital prescription surveillance [17]. The allergen landscape of crabs, other decapod species, and desert mugwort has been mapped as well, providing a foundation for more personalized and component-resolved diagnostic approaches [16, 18, 19]. In addition, a highly sensitive and robust gluten detection platform using a novel alpaca-derived polyclonal antibody has been developed, addressing key limitations of conventional immunoassays [20]. Among house dust mite (HDM)-sensitized patients, reactivity varies between major (e.g., Der p 1/2/23) and minor (e.g., Der p 5/7/10/21) allergens. Xu et al. showed that native HDM allergen extract confers the effectiveness of subcutaneous immunotherapy benefits in Chinese AR patients, irrespective of co-sensitization to major HDM allergens [21]. Evaluation of immunotherapy treatment response has conventionally relied on measuring antigen-specific immunoglobulin E (IgE) and IgG4 [22]. At the cellular level, Ma et al. demonstrated that the combination of type 2 switched memory B-cell frequency and specific-IgE/total-IgE ratio can predict outcome in HDM-sensitized AR patients receiving subcutaneous immunotherapy (SCIT) [23]. Likewise, novel innate type 9 lymphoid cells (ILC9s) are elevated in AR patients' nasal mucosa and blood, decline after HDM-SCIT, and normalize in treatment responders, highlighting their potential role as a biomarker of successful SCIT [24]. This was the first demonstration of human type 9 ILCs a study performed in Davos and Guangzhou. This new ILC9 subset displays Bach2 as a transcription factor, and IL-9 expression decreases after siRNA inhibition of Bach2. Histamine seems to be an important regulator, because ILC9 production increases in response to histamine. An up-regulation of PPARγ was observed in ILCs in response to IL-4 and TGF-β, and ILC9 differentiation was suppressed by the PPARγ antagonist. Physiologically, eosinophils support murine hematopoietic stem cell homeostasis and regeneration [25]. In allergic diseases, their heterogeneity expands. Cai et al. recently used single-cell RNA-seq to define two distinct blood eosinophil subsets in AR, including a disease-associated population characterized by tumor necrosis factor (TNF) responsiveness, upregulated pro-inflammatory and chemotactic gene expression, and low proliferative activity [26]. In asthma, the pathogenic potential of eosinophils is further enhanced by the complement system. Studies have shown that macrophages, as the primary source of the complement component 5 (C5), recruit and activate eosinophils, thereby amplifying eosinophilic inflammation in IL-5 transgenic mouse models [27]. Targeting this pathway, the lectin complement initiator ficolin-A reduces the number of lung eosinophils and inflammation in asthmatic mice [28]. In addition, CD207+ dendritic cells enriched in intraepithelial compartments act as antigen-presenting cells that bridge IL-25 signaling and Th2 polarization in asthma [29]. The focus of Chinese scientists on metabolic regulation of allergic inflammation has identified an important role for the metabolism–remodeling interaction in type 2 upper airway disease in several recent papers [30-32]. Besides that, modulating secondary bile acids may help prevent or alleviate allergic diseases [30]. Considering the finding that metabolic pathways such as the tricarboxylic acid cycle, glycolysis, and propanoate metabolism are enriched in the olfactory bulb of AR mouse models with olfactory impairment [31], further understanding metabolic pathways may unveil new therapeutic targets for allergic airway diseases. The authors have nothing to report. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.