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Journal articleBush A, Chotirmall SH, Han MK, et al., 2026,
To the airway and beyond: introduction to an AJRCCM special section on airway disease.
, Am J Respir Crit Care Med, Vol: 212, Pages: 1879-1881 -
Journal articleMassenet T, Stefanuto P-H, Peltrini R, et al., 2026,
Eosinophil-derived breath biomarkers and response to anti-IL-5/5R biologics in severe asthma.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2075-2078 -
Journal articleSiddiqui S, Brooks L, Menzies-Gow A, et al., 2026,
Prioritizing efficacy over convenience.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2111-2112 -
Journal articleBaraldi F, Mah JSY, Almuhanna A, et al., 2026,
Mucus plug formation is associated with eosinophilic activation in chronic obstructive pulmonary disease.
, Am J Respir Crit Care Med, Vol: 212, Pages: 2071-2074 -
Journal articleNguyen TH, Akdis CA, Baccarelli A, et al., 2026,
Leveraging Artificial Intelligence in Allergy, Asthma, and Immunology With Environmental Exposures.
, Allergy, Vol: 81, Pages: 3130-3145Artificial intelligence (AI) in environmental health science is revolutionizing data analysis and problem-solving approaches. These technologies facilitate the prediction of environmental exposures and disease outcomes and enable the identification of causal relationships for subsequent hypothesis testing. AI techniques improve pollution research through the analysis of satellite imagery and the modeling of pollutant dispersion, while AI advances chemical safety evaluations in toxicology by examining extensive datasets. AI is instrumental in addressing pressing environmental challenges, including remediation of polluted sites and ensuring equitable healthcare applications to mitigate biases. The expanding availability of large-scale environmental, geospatial, and health outcome databases offers unprecedented opportunities for innovative applications. Their predictive capabilities are essential in disaster management, enabling real-time analysis and optimizing resource deployment amid climate-related crises. AI-driven approaches play a critical role in carbon capture and waste management efforts aimed at reducing environmental impact. Furthermore, AI can elucidate complex relationships between the exposome-defined as the totality of exposures throughout an individual's life-and health outcomes, facilitating preventative strategies. This review examines the capabilities and limitations of AI in environmental health and safety, providing insights into its judicious and effective use for environmental management and healthcare.
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Journal articleWang L, Ntotsis K, Manifield J, et al., 2026,
Validation of the General Practice Physical Activity Questionnaire after severe COVID-19.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541BACKGROUND: Physical inactivity is a risk factor for severe COVID-19 and often worsens after hospitalisation. Clinicians need quick, accurate assessments to target interventions. We aimed to assess the validity of the General Practice Physical Activity Questionnaire (GPPAQ) in adults recovering 1 year after COVID-19 hospitalisation. METHODS: Post-hospitalisation for COVID-19, adults attended a 1-year-visit and completed the GPPAQ Physical Activity Index (PAI-4 active), 14-day wrist-worn accelerometry (moderate-vigorous physical activity (MVPA) active) and other health outcomes. Validity was examined via 1) internal consistency (factor analysis); 2) measurement invariance across sex, age and ethnicity using differential item functioning (DIF); 3) convergent validity (GPPAQ sensitivity/specificity versus accelerometry); and 4) construct validity (correlations with health outcomes). RESULTS: 752 participants had GPPAQ and accelerometry (265 female, mean±sd age 60.9±11.6 years), MVPA 18.75 min·day-1 (interquartile range 7.55-36.11), PAI-1 46.8%, PAI-2 15.6%, PAI-3 19.4% and PAI-4 18.2%. Factor analyses supported good internal consistency with two factors (daily activities and physical exercise). Comparative factor index (CFI) showed an excellent fit (CFI 0.965). DIF indicated moderate variability by sex and age. GPPAQ-PAI showed limited sensitivity (26.3%) for correctly classifying physically active individuals, but higher specificity (88.4%) for classifying physical inactivity, and weak-to-moderate correlations with health outcomes. CONCLUSIONS: GPPAQ demonstrates internal consistency, with construct and convergent validity in adults 1 year after COVID-19 hospitalisation. GPPAQ effectively identifies inactive individuals to support clinical care; however, its sensitivity suggests under-estimation of activity relative to accelerometry. Future pathways should combine GPPAQ with device-based assessment to optimise evaluation of physical activity to gu
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Journal articleSong W-J, Kermani NZ, Versi A, et al., 2026,
Clinical Features of Cellular Senescence Pathways in Severe Asthma.
, Allergy, Vol: 81, Pages: 3273-3285BACKGROUND: Asthma severity increases with age, suggesting a role for accelerated biological ageing. We hypothesised that cellular senescence pathways such as the senescence-associated secretory pathway (SASP) and the p53-cellular senescence pathway are enriched in the airways of patients with severe asthma. METHODS: We utilised transcriptomic data from the U-BIOPRED cohort to analyse enrichment scores (ES) of p53 and SASP pathways in different airway compartments using gene set variation analysis. Findings in bronchial biopsies were validated in the independent NOVA cohort. We examined associations between senescence ES, clinical parameters and other asthma-related gene signatures. Functional clusters of the SASP gene set were also explored. RESULTS: In the U-BIOPRED cohort, p53 and SASP ES were significantly elevated in bronchial biopsies of severe asthmatics compared to mild-to-moderate asthmatics and healthy volunteers, with SASP enrichment validated in the NOVA cohort. In bronchial biopsies, higher senescence ES correlated with frequent exacerbations, oral corticosteroid use, comorbid nasal polyps and lower FEV1%. No significant enrichment was found in other airway samples according to asthma severity. In nasal brushings, SASP ES was significantly higher in participants with comorbid nasal polyps. A distinct SASP functional cluster related to lung injury and repair (Cluster 2) was strongly associated with clinical severity and nasal polyps. Senescence signatures correlated positively with oxidative phosphorylation and macrophage activation signatures, but not with eosinophil signatures. CONCLUSIONS: Cellular senescence pathways are enriched in severe asthmatic bronchial tissues and correlate with disease severity, remodelling and nasal polyps. These findings warrant further investigation into their therapeutic implications. TRIAL REGISTRATION: NCT01982162.
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Journal articleScheire S, Lourijsen E, Blauwblomme M, et al., 2026,
Meta-Analysis on the Harm of Systemic Glucocorticosteroids in Inflammatory Upper Airway Disease and Asthma: An EAACI Task Force.
, Allergy, Vol: 81, Pages: 3071-3106Systemic glucocorticosteroids (sGCS) are widely used in the treatment of chronic inflammatory airway diseases such as rhinitis, rhinosinusitis and asthma. It is well-known that systemic use is linked to multiple adverse effects (AEs) both in the short- and the long-term. However, less is known about the safety of multiple short courses of sGCS. Currently there is no established agreement on the acceptable cumulative exposure to sGCS, considering the potential for various AEs. This systematic review and meta-analysis evaluated sGCS-related AEs in both upper and lower inflammatory airway disease, with a particular focus on short- and long-term risks. We further evaluated whether a dose-response relationship existed between the daily and cumulative dosages of sGCS and the occurrence of those AEs. Our meta-analysis confirmed that cumulative dosages between 500 mg and 1 g prednisolone-equivalent significantly increase the risk of most AEs, with risks increasing with incremental dose. These findings underscore the importance of: (a) judicious sGCS prescription and need for steroid stewardship, due to their potential for short- and long-term complications, occurring even with repeated short courses, and (b) prioritization of steroid-sparing approaches (e.g., biologicals) to avoid reaching a cumulative dose of 500 mg.
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Journal articleBousquet J, Ventura MT, Taborda-Barata L, et al., 2026,
Allergic Rhinitis in the Elderly: In Collaboration With the ARIA Guidelines.
, J Allergy Clin Immunol Pract, Vol: 14, Pages: 1963-1979Rhinitis in the elderly represents a unique challenge, due to specific clinical profiles, needs, and expectations. Allergic rhinitis (AR) in the elderly is often intertwined with nonallergic rhinitis. Multimorbidity, frailty, disability, and polypharmacy leading to drug-drug interactions are all important in the elderly. Epidemiological data remain limited. AR in the elderly often follows an earlier onset, but some patients may start AR symptoms later. Rhinitis in the elderly is often underrecognized because the symptoms are those of AR possibly combined with nonallergic rhinitis influenced by age-related structural and functional changes in the nose. These include nasal dryness, congestion without clear trigger, and rhinorrhea alone. Several characteristics of AR in the elderly render AR diagnosis more challenging in this age group. An assessment of control and severity is needed to optimize person-centered treatment. There is no specific guideline for the management of AR in the elderly. However, although AR in the elderly may differ from rhinitis in younger adults, and medication efficacy may be reduced, the main management trend is the same as that in younger patients. The key problem is safety, because some drugs may cause specific severe side effects. First-generation oral antihistamines should be avoided. Intranasal corticosteroids, second-generation oral antihistamines, as well as intranasal H1-antihistamine and intranasal H1-antihistamine-intranasal corticosteroid fixed combination are the first-line therapeutic options. Digital health associated with artificial intelligence has a promising future for AR management.
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Journal articlePiga NN, Portelli MA, Shrine N, et al., 2026,
Genome-wide association study of asthma with high treatment burden and/or worse outcomes defined using electronic healthcare data in UK Biobank.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541BACKGROUND: In ∼10% of asthma patients, symptoms remain uncontrolled despite maximal treatment, representing an unmet clinical need. The causal variants, genes and pathways underlying genetic risk factors have not been fully elucidated, and it is unclear whether there are unique genetic risk factors for this asthma subtype. METHODS: We used electronic healthcare records linked to UK Biobank to identify asthma patients with high treatment burden and/or worse outcomes. We performed a genome-wide association study (GWAS) with this case population and healthy controls. We sought replication for associated (p≤5×10-6) signals in four independent studies (12 152 cases and 32 316 controls). Replicated signals were fine-mapped and linked to genes and pathways. RESULTS: In total, 7681 participants met our case definition and showed enrichment for adult-onset asthma, female gender and higher body mass index compared to asthma individuals not meeting case criteria. GWAS with 7681 cases and 38 405 controls revealed 21 reproducible association signals that had previously been associated with asthma, but had a larger effect size in our study. Variant-to-gene mapping highlighted 85 candidate genes, five of which were considered high confidence (BACH2, D2HGDH, IL1RL1, RPS26, SMAD3). CONCLUSION: We present the first use of electronic healthcare records in UK Biobank to identify a subtype of asthma enriched for patients with high treatment burden and/or worse outcomes. Our findings support the role of known asthma genes, highlighting genetic risk variants with stronger effect in these groups of patients. The prioritised genes provide potential therapeutic opportunities for this difficult-to-treat patient population.
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Journal articleSiddiqui S, Ding B, Dolin P, et al., 2026,
Epidemiology, clinical management, and outcomes in patients with eosinophilic granulomatosis with polyangiitis in England: A retrospective observational cohort study.
, J Allergy Clin Immunol Glob, Vol: 5BACKGROUND: Data on the clinical burden of eosinophilic granulomatosis with polyangiitis (EGPA) are limited. OBJECTIVE: We sought to evaluate the epidemiology and clinical burden of EGPA in England using real-world evidence. METHODS: Patients diagnosed with EGPA between January 1, 2006, and February 28, 2019, who had ≥1 year of data before diagnosis (index date) were identified using the Clinical Practice Research Datalink Aurum database. Epidemiology, diagnosis, mortality, treatment, and clinical outcomes were assessed. RESULTS: The incident and prevalent EGPA cohorts comprised 486 and 729 patients, respectively. The overall incidence and prevalence of EGPA were 3.04 (95% CI: 2.77-3.32) cases per million person-years and 2.7 (95% CI: 2.5-2.9) cases per 100,000 persons, respectively. Overall, 76.3% and 26.1% of patients had a Five Factor Score of 0 on the 1996 and 2009 versions. In the incident cohort (mean age 57.9 ± 15.2 years), most patients (97.1%) had ≥1 comorbidity; 79.8% had asthma coded. The median time from first major manifestation to EGPA diagnosis was 44.0 (Q1-Q3: 20.0-56.0) months. The death rate was 37.1 per 1000 person-years (95% CI: 30.1-45.2); the standardized mortality ratio for all-cause deaths was 2.3 (95% CI: 1.9-2.8). The 5-year survival rate was 82.3% (95% CI: 78.1%-85.7%). Most patients (86.2%) received oral glucocorticoids, of whom 27.0% successfully tapered. Six months post index date, 26.1% of patients had a new EGPA manifestation. CONCLUSION: This study emphasizes the substantial clinical burden and reliance on glucocorticoids in EGPA, highlighting the need for improved diagnosis of this disorder.
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Journal articleYang F, Seo S, Hasegawa T, et al., 2026,
Longer Asthma Duration Is Associated With Elevated Non-T2 Sputum Biomarkers and Reduced T2 Inflammation in Severe Asthma.
, Allergy, Vol: 81, Pages: 3286-3299BACKGROUND: Longer asthma duration predicts non-remission in Type-2 (T2) biologic-treated severe asthma, but underlying mechanisms remain unclear. We investigated associations between asthma duration and inflammatory biomarkers that may explain differential biologic response. METHODS: We analysed cross-sectional data from adults with severe asthma in U-BIOPRED. Asthma duration was defined as years from diagnosis to study entry. T2 and non-T2 biomarkers were measured in blood and sputum. Identical assays were performed in PRISM, a validation cohort of biologic-initiators. Multivariable regression models adjusted for age, sex, ethnicity, BMI, smoking and oral corticosteroid dose. Associations between duration-related biomarkers and 12-month biologic remission were explored in PRISM. RESULTS: In U-BIOPRED (n = 411), median asthma duration was 23 years (IQR 12-38). Longer duration was associated with higher non-T2 biomarkers including sputum CXCL9 (β = 0.024, 95% CI 0.011-0.038), sputum IL-6 (β = 0.024, 95% CI 0.011-0.037) and sputum neutrophils (β = 0.009, 95% CI 0.001-0.017), but lower T2 biomarkers including plasma periostin (β = -0.006, 95% CI -0.009 to -0.003), eosinophils (blood: β = -0.002, 95% CI -0.003 to -0.001; sputum: β = -0.023, 95% CI -0.035 to -0.011), sputum EDN (β = -0.032, 95% CI -0.049 to -0.014) and FeNO (β = -0.006, 95% CI -0.010 to -0.001). PRISM (n = 474) confirmed these associations. Higher sputum CXCL9 was associated with reduced remission in anti-IL-4Rα-treated patients with asthma duration ≥ 20 years (β = -1.73, 95% CI -3.180 to -0.276). CONCLUSION: Longer asthma duration was associated with elevated airway non-T2 inflammation and reduced systemic and airway T2 inflammation. This highlights the importance of airway bio
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Journal articleShih Y-S, Han C-L, Lee YL, et al., 2026,
Extreme temperature and airway dehydration: current understanding and integrative insights into respiratory vulnerability.
, Expert Rev Respir Med, Vol: 20, Pages: 1055-1066INTRODUCTION: Climate change has significantly increased the frequency and intensity of extreme temperature events, posing growing threats to respiratory health. Among the underlying mechanisms, airway dehydration is a critical yet underrecognized pathway that disrupts the airway surface liquid (ASL), which is essential for mucociliary clearance, epithelial integrity, and immune defense. AREAS COVERED: This article examines evidence linking airway dehydration to respiratory disease during temperature extremes. We discuss how hot, dry air and cold, low-humidity conditions disrupt airway hydration balance, leading to impaired mucociliary clearance and increased susceptibility to infection and inflammation. The review summarizes the impacts of airway dehydration on vulnerable populations, including individuals with pre-existing respiratory conditions (asthma, allergic rhinitis, chronic obstructive pulmonary disease (COPD), and cystic fibrosis), children, older adults, outdoor workers, and socioeconomically disadvantaged groups. EXPERT OPINION: Airway dehydration represents a unifying mechanism linking climate extremes to respiratory vulnerability but remains underrepresented in clinical practice and public health strategies. We advocate for greater recognition of airway hydration in disease prevention, development of practical measurement tools, and targeted interventions for at-risk populations. Emphasizing airway dehydration as a key mediator offers opportunities to improve clinical management and develop effective climate adaptation strategies for respiratory health protection.
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Journal articleShen J, Chaudhuri R, Bicknell S, et al., 2026,
The Airway Transcriptome in Type 2 Cytokine Biomarker-High and -Low Severe Asthma.
, Allergy, Vol: 81, Pages: 3300-3317Severe asthma is a heterogeneous disease. The mechanisms driving airway pathology when type 2 (T2) cytokine activity is suppressed remain poorly understood. This study aimed to provide insight by identifying the airway molecular pathways of T2 biomarker-high and -low severe asthma. We analysed clinical and transcriptomic data from bronchial biopsies and brushes in the UK Refractory Asthma Stratification Programme multi-centre severe asthma cohort (18 corticosteroid-resistant T2 biomarker-high [T2-high], 23 T2 biomarker-intermediate [T2-intermediate], 11 T2 biomarker-low [T2-low]) plus 20 healthy controls pre- and post-treatment with high-dose inhaled corticosteroids (ICS). Many genes dysregulated in asthma vs. health were concordantly dysregulated in healthy subjects receiving ICS. Severe asthma as a whole, independent of confounding by ICS, was characterised by upregulation of mucins, CEACAM5, typical T2-genes (POSTN, CLCA1, CCL26), epithelial mast cell genes, and CPA4. T2-high severe asthma demonstrated upregulated T2-dependent genes, epithelial barrier and keratin genes, adaptive immune responses, and impaired ciliary function. T2-low asthma showed upregulated Th1- and IL-17-associated genes (IDO1, CXCL10, GBP1, LAG3), interferon-γ signalling, neuroimmune pathways, airway smooth muscle-related genes, and neutrophil enrichment. T2-intermediate asthma exhibited a mixed molecular profile sharing features of T2-high and T2-low endotypes, with selective expression of the pathogen defence and antiviral response genes. The results were validated using bronchoscopy data from the U-BIOPRED Consortium. This study defines airway molecular endotypes of severe asthma associated with T2 biomarker high and low phenotypes, independent of corticosteroid effects. These findings offer insights for severe asthma management and the development of targeted biologic therapies.
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Journal articleTorres MJ, Shamji M, Arasi S, et al., 2026,
Decalogue of the Declaration of Salamanca: Advancing Undergraduate Education in Allergy and Clinical Immunology Across Europe.
, Allergy, Vol: 81, Pages: 3035-3038 -
Journal articleMatīsa D, Bansal AT, Rink S, et al., 2026,
Managing multimorbidity in severe asthma: comparison of resources and perspectives between severe asthma specialists and general respiratory physicians across Europe.
, ERJ Open Res, Vol: 12, ISSN: 2312-0541BACKGROUND: Multimorbidity refers to the presence of multiple coexisting conditions, but is often underappreciated in the context of severe asthma (SA) management. We sought to identify differences in approaches to multimorbidity management in SA, variability in access to multidisciplinary team (MDT) resources, and whether physician perspectives on multimorbidity differ between SA specialists and general respiratory physicians. METHODS: The Severe Heterogeneous Asthma Registry, Patient-centred (SHARP) Clinical Research Collaboration circulated an online physician survey via European national respiratory societies to assess 1) available resources to address multimorbidity and 2) physician perspectives on multimorbidity in SA. RESULTS: 495 responses from 25 European countries included 48% SA specialists and 52% general respiratory physicians. SA specialists had more experience with SA patients (20% were seeing >60 patients per month) compared to general respiratory physicians. SA specialists had greater access to multidisciplinary care - including better access to MDTs, allied health professionals and referrals to external specialists, and therefore more routinely assessed comorbidities and considered them greater influences on their practice. They also considered multimorbidity to a greater degree and rated its impact on their patients' asthma outcomes (and general health outcomes) as more substantial. CONCLUSIONS: Alongside more experience of treating SA, SA specialists have increased awareness of multimorbidity and better resources to manage it. However, access to MDTs remains a significant gap for both SA specialists and general respiratory physicians. Furthermore, both groups identified a high need for further education and training about multimorbidity. These findings highlight key areas for improvement in clinical practice, resources and training.
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Journal articleShamji MM, Rider NL, Adcock I, et al., 2026,
PRACTALL 2025: Artificial intelligence-application of allergy and immunology to patient care.
, J Allergy Clin Immunol, Vol: 158, Pages: 694-714Artificial intelligence (AI), first defined in 1955 by John McCarthy, has transformed daily life across industries through applications such as chatbots, autonomous vehicles, and navigation systems. The 2022 release of ChatGPT marked a pivotal moment, highlighting AI's rapidly expanding potential. The health care industry is increasingly embracing AI-enabled tools across oncology, pathology, and radiology to augment disease screening and clinical workflows. Ambient listening technologies support clinical documentation, reduce administrative burden, and improve patient-physician interactions. Large language models combined with natural language processing are being evaluated for generating clinical summaries managing patient portal messaging and converting freehand notes to electronic health records, while also uncovering patterns in patient data to support more personalized treatments. Forward-thinking health systems are establishing informatics departments to optimize these models. Notably, with 1 in 6 adults sourcing health information from AI, rising to nearly one-quarter among individuals younger than 30 years, there is a growing need to ensure that these technologies provide accurate and reliable information to safeguard patient safety and support appropriate clinical use. PRACTALL, a collaboration between the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy & Clinical Immunology, aims to equip allergist-immunologists with essential AI insights highlighting tools for clinical practice, education, and research. By addressing potential pitfalls and biases, PRACTALL illustrates how AI can enhance efficiency, improve patient care, and alleviate administrative burdens in health care.
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Journal articleKumar A, Chan R, Zounemat-Kermani N, et al., 2026,
Small Airways Dysfunction and Remission in Adults With Asthma: A Longitudinal Exploratory Analysis of the AssessmenT of smalL Airways involvemeNT In aSthma (ATLANTIS) Study.
, Allergy, Vol: 81, Pages: 3185-3196BACKGROUND: Asthma remission is a feasible treatment goal. However, remission definitions vary, and predictive biomarkers remain underexplored. METHODS: We conducted a post hoc analysis of ATLANTIS (NCT02123667), a multinational prospective study including 684 adult asthmatics. Remission was defined by 3-component (3C) and 4-component (4C) criteria. 3C remission included: (1) ACQ-6 < 1.5, (2) no maintenance oral corticosteroids, (3) no exacerbations. An absolute decline < 10% in pre-bronchodilator FEV1% predicted, was added for the 4C definition. Multivariate logistic regression identified remission predictors. A novel Low Disease Activity (LDA) score was developed using factor analysis of five clinical variables (ACQ-6, FeNO, BEC, and FEV1) including an innovative small airways dysfunction questionnaire tool (SADT). Nasal transcriptomics were analysed for differential gene expression and pathway enrichment and were replicated in U-BIOPRED (NCT01976767) using sputum transcriptomics. U-BIOPRED was included only to study omics replication of remission pathways identified in ATLANTIS. FINDINGS: Remission occurred in 48% (3C) and 45% (4C) of patients. Predictors included male sex, better lung function, fewer previous exacerbations, and higher SADT (fewer small airways symptoms). LDA identified milder disease and was associated with remission [OR 3C 4.43 (2.80, 7.10) and 4C 3.46 (2.23, 5.43)], improved QoL [OR 2.07 (1.65, 2.60)], and fewer future exacerbations [OR 0.43 (0.22, 0.85)]. Transcriptomic analyses revealed remission-associated upregulation of interleukin 4/13 signalling and downregulation of coagulation pathways, in both ATLANTIS and U-BIOPRED. INTERPRETATION: SAD was associated with reduced asthma remission. A novel LDA tool demonstrated clinical utility in stratifying prospective asthma risk. Key immunologic and haemostatic pathways may underpin remission, offering potential targets for future intervention.
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Journal articleDeBerg HA, Baloh CH, DeGottardi Q, et al., 2026,
Differential effects of subcutaneous and sublingual immunotherapy on timothy grass-specific TH2 CD4+ T-cell subsets.
, J Allergy Clin Immunol, Vol: 158, Pages: 845-856BACKGROUND: Allergen-specific CD4+ T cells are a highly heterogenous population. Depletion of these cells has been proposed as essential to achieve allergen desensitization in allergen immunotherapy. OBJECTIVE: The overall aim of this study was to characterize the heterogeneity of timothy grass (Phleum pratense) allergen-specific CD4+ T cells and determine how the frequency and phenotype of these cells change in response to sublingual (SLIT) and subcutaneous (SCIT) immunotherapy. Correlations between frequencies of these cells with Total Nasal Symptom Score and grass-specific serum immunoglobulin were also investigated. METHODS: Mass cytometry with lanthanides-tagged peptide major histocompatibility complex class II multimers and CD154 upregulation assays were used to examine changes in the frequency and phenotype of Phl p-specific CD4+ T cells in longitudinal peripheral blood mononuclear cell samples from a randomized, double-blind, placebo-controlled trial of SLIT and SCIT. Supervised and unsupervised clustering was used for data analysis. RESULTS: Phenotypes of Phl p-specific T cells were highly heterogenous but could be categorized into two major metaclusters, CRTH2hiCD27lo and CRTH2loCD27hi, each with distinct phenotypic profiles. Weak positive correlations between Total Nasal Symptom Score and frequencies of T cells within both subsets were observed. SCIT preferentially depleted CRTH2hiCD27lo cells, whereas SLIT depleted CRTH2loCD27hi cells. CRTH2hiCD27lo cell frequency correlated with Phl p-specific IgE and IgG4, but not IgA, levels. CONCLUSION: Unsupervised clustering revealed distinct subpopulations of allergen-specific T cells that were differentially targeted and depleted by SCIT and SLIT, suggesting that SCIT and SLIT act through overlapping but distinct immunologic pathways.
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Journal articleSiddiqui SH, Ding B, Dolin P, et al., 2026,
Healthcare resource utilisation and associated costs in patients with eosinophilic granulomatosis with polyangiitis in England: A retrospective observational cohort study.
, World Allergy Organ J, Vol: 19, ISSN: 1939-4551BACKGROUND: Real-world data on the healthcare resource utilisation (HCRU) and cost burden of eosinophilic granulomatosis with polyangiitis (EGPA) are limited. We assessed all-cause HCRU and costs in patients with EGPA versus a matched general population cohort without EGPA and a severe uncontrolled asthma (SUA) cohort. METHODS: Primary care data in England from the Clinical Practice Research Datalink Aurum database, with linkage to Hospital Episode Statistics inpatient, outpatient and emergency department records, were analysed. Patients with a new EGPA diagnosis in 2006-2020 and ≥ 1 year of data before diagnosis (index date [ID]) were included and matched using a matching ratio of up to 1:4 with a general population cohort without EGPA and patients with SUA. Follow-up was from ID until deregistration, last data collection, death or study end. HCRU and associated costs were assessed across the 12 months prior to ID, and annually from ID to end of the study period, and by disease states and Five-Factor Score [FFS]. RESULTS: A total of 486 patients with EGPA were identified, with a corresponding matched general population cohort of 1938 and SUA cohort of 1005 patients. Annual all-cause HCRU rates during follow-up were higher in the EGPA cohort versus the general population and SUA cohorts for all types of care, particularly in the first year after ID. Patients with an FFS of 0 generally had lower HCRU than those with an FFS ≥1. Annualised total HCRU-associated costs (95% confidence interval [CI]) were higher in the EGPA cohort (£13,978 [12,068, 15,888]) versus the general population (£2303 [2145, 2461]) and matched SUA cohorts (£3571 [3326, 3816]), with cost ratios (95% CI) of 8.3 (7.1, 9.6) and 4.1 (3.6, 4.6) respectively, both p < 0.0001. The greatest cost driver was hospital admissions with cost ratios (95% CI) of 12.3 (9.8, 15.5) and 5.8 (4.7, 7.2) compared with the general population and SUA cohorts, respectively. Median all-cause annua
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