Allergic rhinitis (AR) is a common and increasingly prevalent chronic inflammatory disorder of the nasal mucosa that severely impacts patients’ quality of life, causing symptoms like nasal congestion, sneezing, and itching. AR is primarily mediated by immunoglobulin E (IgE) when allergens are present, making it challenging to manage despite available therapies like pharmacotherapy, immunotherapy, and surgery. Recently, research has focused on biologics as an emerging therapeutic option for AR. Biologics target specific immune pathways in type 2 inflammation, which underlies many allergic diseases including AR. Biologics offer a targeted and potentially more effective alternative to traditional therapies, addressing the underlying immune mechanisms rather than simply alleviating symptoms. Based on key clinical trial evidence, this paper tentatively proposes a multidimensional strategy for selecting biologics in AR, integrating serum IgE levels, disease phenotypes (seasonal/persistent), and comorbid characteristics to guide individualized treatment. However, the long-term cost-effectiveness, optimal dosing regimens, and patient adherence to biologics require further validation through real-world data. Despite these challenges, recent advancements in biologics represent a promising step forward in AR management. With ongoing research and clinical trials, biologics may soon provide more effective and lasting relief for patients suffering from allergic rhinitis.

Objective: The relationship between vascular compression of the vestibulocochlear nerve and audio-vestibular symptoms remains controversial. We aimed to examine the radiological features of vascular loops signs in cerebellopontine angle (CPA) and internal auditory canal (IAC) in patients with unilateral Ménière’s disease (MD). Methods: One hundred and thirty-seven patients with unilateral definite MD and 69 control subjects (138 ears) were enrolled. All subjects received magnetic resonance imaging of CPA-IAC. The configuration of vascular loops in CPA-IAC, based on the Kazawa classification system, from MD-affected, non-affected and control ears were compared. The associations between imaging findings and Ménière’s stage, electrocochleogram (EcochG) and caloric test were analyzed. Results: (1) Among the MD-affected ears, 6 cases (4.4%) were classified as Kazawa type IA, 27 cases (19.7%) as IB, 60 cases (43.8%) as IIA, and 44 cases (32.1%) as IIB. No significant interaural difference in the distribution of Kazawa's types was found ( $${x}^{2}$$x 2 = 4.737, p = 0.578) in unilateral MD patients. (2) The distribution of Kazawa's types were not significantly different between the MD-affected ears and the control subjects ( $${x}^{2}$$x 2 = 2.876, p = 0.411). (3) No relationship was found between Kazawa staging of the MD-affected ear and Ménière’s stage (H = 2.679, p = 0.444), EcochG ( $${x}^{2}$$x 2 = 0.827, p = 0.867) and caloric test ( $${x}^{2}$$x 2 = 4.116, p = 0.248). Conclusions: In patients with unilateral MD, the configuration of vascular loops in CPA-IAC region, measured by Kazawa criteria, did not correlate with the laterality, clinical stage, the results of EcochG and caloric test, suggesting that vascular loops may be natural anatomical variations for patients with MD.

Background: It has been reported that when DCs are exposed to high-dose antigens, they can induce Th0 cells into regulatory cells (Treg) and Th1 cells. When DCs are subjected to low-dose allergen, they can drive to Th2 cells. However, the mechanisms of such dose-effect relationship are poorly understood so far. Methods: Bone marrow immature DCs (imDCs) were generated from mice and stimulated with OVA of different concentrations (0, 10, 100, 1000, 10000 μg/ml, respectively). The mDCs were then seeded and cocultured with naïve T cells for 3 days, and then the markers of different T cell subgroups were flow cytometrically tested. RNA-seq detection and DNA methylation of DCs were performed. Results: When DCs were stimulated with low-dose (10ug/ml), 77 genes were up-regulated and 87 genes down-regulated. Most activated genes were related to ribosome synthesis and ion channel inhibition but not to the immune responses and Th2 activation. At the medium-dose (100μg/ml), 339 genes were up-regulated and 168 genes down-regulated. Most activated genes involved cytokine synthesis and regulation of immune responses. At high-dose (10000μg/ml), 2794 genes were up-regulated and 1156 genes down-regulated. Tumor necrosis factor signaling pathway, MAPK signaling pathway, antigen processing and presentation signaling pathway were mostly up-regulated. The related co-stimulators, co-inhibitory molecules, inhibitory cytokines, negative regulating enzymes were highly expressed. The monocarbate, coenzyme, fatty acid, glucolipid, starch, sucrose and other metabolism-related signaling pathways were down-regulated. Conclusion: The profiles of DNA methylation and RNA synthesis of DCs varied with different doses of OVA, which serves to induce T cells to differentiate in various directions.

Background: Stapokibart is a novel biologic for chronic rhinosinusitis with nasal polyps (CRSwNP). We aimed to identify baseline biomarkers predicting early (4-week) and mid-term (16-week) responses to stapokibart in CRSwNP. Methods: A total of 57 patients were prospectively enrolled. Baseline clinical data and complete blood count (CBC) parameters were collected, and derived inflammatory indices were calculated. Patients were classified as responders or non-responders at week 4 and 16 based on achieving either a ≥8.9-point reduction in SNOT-22 or a ≥1-point decrease in Nasal Polyp Score (NPS). Results: Stapokibart significantly improved SNOT-22, VAS, and NPS at both week 4 and week 16 (all p < 0.001). At week 4, 80.7% achieved an early response. Responders showed significantly higher baseline eosinophil count and eosinophil percentage and lower neutrophil-to-eosinophil ratio (N/E) (all p < 0.05). Univariate analysis identified N/E, comorbid asthma, eosinophil count, and aggregate index of systemic inflammation (AISI) as predictors of early response (all p < 0.05). Multivariate analysis identified N/E as an independent predictor (OR = 0.943, p = 0.011; AUC = 0.756). At week 16, 75.4% of patients achieved a mid-term response. Responders had significantly higher baseline SNOT-22 scores and NPS (p < 0.05). Multivariate analysis showed that baseline NPS and SNOT-22 scores were independently associated with mid-term response, and their combined model showed good predictive performance (AUC = 0.832, 95% CI: 0.716–0.948). Conclusions: Peripheral blood inflammatory biomarkers, particularly N/E, may predict early response to stapokibart in CRSwNP, whereas mid-term response appears more strongly associated with baseline disease severity. These findings support biomarker-driven stratification for individualized treatment strategies in CRSwNP.