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Journal articleFreeman A, Rink S, Bansal AT, et al., 2026,
Multimorbidity phenotypes and associated characteristics in severe asthma: an observational study of European severe asthma registries.
, Lancet Reg Health Eur, Vol: 63BACKGROUND: The phenotypic nature of multimorbidity in severe asthma is poorly understood. Our aims in this study were to define multimorbidity phenotypes and their characteristics in severe asthma across Europe by identifying and characterising co-aggregation of comorbidities. METHODS: Cross-sectional patient data were analysed from the pan-European Severe Heterogenous Asthma Research Collaboration: Patient Centred (SHARP) Central database of national severe asthma registries. Patients were grouped by four European regions (North, South, East, and West). Hierarchical clustering of comorbidities was applied to characterise the correlation structure of the ten commonest comorbidities within these geographical regions. Subsequent multimorbidity phenotypes (MMP) and their clinical features were then defined. FINDINGS: Data were available for 2690 severe asthma patients and 23 comorbidities from 11 countries. Three comorbidity clusters were consistently seen across the four European regions: 1) osteoporosis plus steroid-induced weight gain, 2) eczema plus rhinitis, and 3) chronic sinusitis plus nasal polyps. Four further comorbidities (obesity, bronchiectasis, gastro-oesophageal reflux disease, psychological factors) showed variable clustering. Multimorbidity was ubiquitous. Patients were assigned multimorbidity phenotypes (MMP) according to comorbidity cluster alignment. MMP sn (sinonasal-associated) and MMP u (no specific cluster alignment) were commonest. MMP ster (steroid-associated multimorbidity) had highest maintenance oral steroid (m-OCS) use, and Body Mass Index, plus worst lung function, asthma control, and asthma exacerbation frequency. MMP max (maximal multimorbidity) showed high prevalence of variably assigned comorbidities, higher m-OCS and biologic treatment needs. INTERPRETATION: Multimorbidity is common in severe asthma and can be classified into replicable novel phenotypes with characteristic clinical traits and outcomes. Recognising these phenotypes c
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Journal articlePuttur F, Lloyd CM, 2026,
Sex Differences in Lung Immunity.
, Immunol Rev, Vol: 338Biological sex has a significant impact on how the immune system develops and responds to foreign and self-antigens. Sex differences exist in innate and adaptive immune cells, both at homeostasis and in the context of infection and inflammatory diseases such as asthma, cancer, and autoimmune disorders. Women generate stronger immune responses and are more susceptible to developing autoimmune conditions, while males are more prone to acute viral infections and developing certain cancers. Some immunological differences persist throughout life, while others emerge only after puberty and before reproductive senescence. Additionally, environmental exposures can affect the influence of biological sex in regulating immune function. This is particularly pertinent at mucosal surfaces such as the lungs, where lung immune defenses are constantly exposed to foreign material during respiration. Consequently, environmental factors together with genetics, age and sex hormones play a vital role in governing lung tissue immune responses between the sexes. In this context, we highlight studies that support the need for considering sex as an important biological variable in lung immunological research. This knowledge will provide a benchmark for understanding sex-driven immunological mechanisms that underpin disease development and may inform new avenues targeted for generating sex-specific therapies in lung disease.
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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.
, AllergyBACKGROUND: 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 articleWang D, Hadad N, Moss S, et al., 2026,
Assessment of mosaic loss of chromosome Y in pulmonary fibrosis reveals limited association with susceptibility or disease severity.
, BMJ Open Respir Res, Vol: 13BACKGROUND: Pulmonary fibrosis (PF) is a rare lung disease with diverse pathogenesis and biological mechanisms. Mosaic loss of chromosome Y (mLOY) has been reported to be associated with increased risk of fibrotic diseases. However, the exact role of mLOY in the development of PF remains to be elucidated. METHODS: Copy number on chromosome Y was used to estimate mLOY comparing patients in PROFILE and gnomAD cohorts and between cases and control patients from the GE100KGP cohort. Correlation of mLOY with demographic and clinical variables was tested using patients from the PROFILE cohort. Lung single-cell transcriptomic data were analysed to assess the cell types implicated in mLOY. Mendelian randomisation was performed to examine the causal relationship between mLOY, idiopathic pulmonary fibrosis (IPF) and telomere length. RESULTS: The genetic analysis suggests that mLOY is found in PF from both case cohorts but when compared with an age matched population the effect is minimal (p=0.00316, median: 0.288 vs 0.291). mLOY is related to age (p=0.000214) and shorter telomere length (p=0.00815) rather than PF severity or progression. Single-cell analysis indicates that mLOY appears to be found primarily in immune cells. Mendelian randomisation demonstrates that mLOY is not on the causal pathway for IPF, but partial evidence supports that telomere shortening is on the causal pathway for mLOY. CONCLUSIONS: Our study confirms the existence of mLOY in PF patients, suggests that mLOY is not a major driver of IPF, and might support a triangulation model where telomere shortening leads to both IPF and mLOY.
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Journal articleKlimek L, Mullol J, Hummel T, et al., 2026,
The Unmet Need of Olfactory Testing in Inflammatory Disorders of the Upper Airways-An EAACI Position Paper.
, AllergyThe sense of smell, with its extensive evolutionary history, is highly prone to disorders that can have a profound impact on daily life. Anosmia affects approximately 5% of the population, with an additional 15% exhibiting reduced olfactory function. The prevalence of olfactory dysfunction (OD) varies by population and age group, and standardized testing reveals a broad range of impacts. OD includes various causes, most commonly aging, inflammation of the olfactory epithelium, upper respiratory tract infections (URTI), traumatic brain injury, and neurological conditions. The recent COVID-19 pandemic has highlighted the association between viral infections and olfactory dysfunction, with severe hyposmia/anosmia being an early marker of infection. Despite its importance, the assessment of olfactory function remains inconsistent across clinical practices. Psychophysical smell tests, while vital for diagnosis and patient management, are underutilized, especially outside of specialized centers. Standardized testing methods are crucial for objective diagnosis, but significant challenges, including test variability, lack of comparability, and healthcare reimbursement issues, persist. The European Academy of Allergy and Immunology (EAACI) advocates for improvements in the quality and standardization of chemosensory assessments. Future efforts must prioritize education, incentives for better testing, and the integration of digital tools to expand access to olfactory testing and diagnosis in remote or quarantine situations. However, office-based testing remains irreplaceable, even with advancements in telemedicine.
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Journal articleSory DR, Heyraud ACM, Jones JR, et al., 2026,
SiO2-CaOCME/Poly(Tetrahydrofuran)/Poly(Caprolactone) 3D-Printed Scaffolds Drive Human-Bone Marrow Stromal Cell Osteogenic Differentiation.
, Adv Healthc MaterThis article addresses the unmet clinical need of scaffolds for bone regeneration that can combine osteogenic properties, such as the promotion of bone marrow stem cell differentiation into osteoblasts, with the ability to withstand cyclic loading. In our previous study, we demonstrated that discs of SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) hybrids or their dissolution products can drive terminal osteogenic differentiation of human bone marrow stromal cells (h-BMSCs) in vitro. The current study shows that the 3D-printed hybrid scaffolds with physiologically relevant 3D architecture further promote h-BMSC osteogenesis. The 3D-printed scaffolds support spatially organized cell behavior in an environment mirroring conditions relevant to off-the-shelf implant applications. Primary cellular functions, including viability, adhesion, and proliferation, were maintained across 3D scaffold surfaces and within inter-strut regions. osteogenic commitment was evidenced by the upregulation of lineage-specific transcripts, hydroxyapatite deposition, and the organized assembly of extracellular matrix (ECM) proteins. Our results demonstrate that 3D-printed scaffolds drive osteogenesis by modulating cell metabolism, inducing osteogenic morphological transitions, and promoting the expression of osteocalcin and collagen type I alpha 1 chain, alongside hydroxyapatite matrix mineralization. Collectively, our findings highlight the SiO2-CaOCME/poly(tetrahydrofuran)/poly(caprolactone) scaffold's strong osteogenic properties-driven by composition, surface architecture, and ion release - and its promise for clinical bone regeneration.
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Journal articleStewart I, John A, Bin L, et al., 2026,
Residual lung abnormality following COVID-19 hospitalisation is characterised by biomarkers of epithelial injury
, EBioMedicine, Vol: 124, ISSN: 2352-3964Some survivors of acute COVID-19 infection have long-term symptoms that could suggest ongoing lung impairment. Searches performed in MEDLINE and Embase for SARS-COV-2 studies with radiological lung follow-up estimated that 50% of participants had inflammatory patterns and 29% had fibrotic patterns at a median of 3 months post infection. Analysis of the UK nationwide Post-hospitalisation COVID-19 Study at 5-months follow-up suggested that up to 11% of people discharged from hospital following COVID-19 infection were at-risk of radiological residual lung abnormalities, such as ground glass opacity and reticulation. In people with pulmonary fibrosis, these radiological patterns are often consistent with persistent epithelial lung injury. Biomarker studies have identified associations with COVID-19 severity, however there are few studies that explore the relationship between biomarkers of epithelial injury and parenchymal lung abnormalities post-hospitalisation.
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Journal articleAlvarez-Paggi D, Ullah A, Ofman G, et al., 2026,
Diagnostic labels and clusters based on oxygen requirements in preterm infants with chronic lung disease: a data-driven exploratory cluster analysis in two independent cohorts.
, Lancet Child Adolesc Health, Vol: 10, Pages: 83-93BACKGROUND: Diagnosis of bronchopulmonary dysplasia in very low birthweight infants is often only ascertained many weeks after birth. We aimed to investigate whether trajectories of the fractions of inspired oxygen (FiO2) required to maintain O2 saturation from birth reflect distinct clusters of preterm lung disease. METHODS: In this data-driven exploratory cluster analysis, we used latent class trajectory modelling to derive clusters of FiO2 fluctuations in the first 30 days of life among neonates with a birthweight of less than 1250 g, across two multicentre, prospective cohorts: the Discovery Bronchopulmonary Dysplasia Program (D-BPD; enrolment July 30, 2013, to Jan 1, 2020; n=376) in Argentina and the Prematurity and Respiratory Outcomes Program (PROP; enrolment Aug 1, 2011, to Nov 31, 2013; n=835) in the USA, with the PROP cohort being used for external validation. Eligible participants, in both the present and original studies, included infants with birthweight of less than 1250 g in the D-BPD cohort, and infants enrolled in the PROP study born at 23-28 weeks of gestation by best obstetrical estimate. After unsupervised clustering of patients, we evaluated cluster performance against conventional bronchopulmonary dysplasia classification, using mortality as the primary outcome. FINDINGS: Of the 376 D-BPD infants, 190 (51%) were female (mean birthweight 968·1 g [SD 181·2]; mean gestational age 28·9 weeks [SD 2·3]) and 186 (49%) were male (mean birthweight 976·2 g [188·3]; mean gestational age 28·6 weeks [2·3]). Four clusters based on FiO2 requirements were identified: persistently low requirement (PLR; 218 [58%] of 376), early high with subsequent improvement (EHRI; 60 [16%] of 376), late-onset high requirement (LOHR; 31 [8%] of 376), and persistently high requirement (PHR; 67 [18%] of 376). Mortality was more frequent in LOHR (six [19%] of 31) and PHR (ten [15%] of 67) clusters, with no deaths in PLR and
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Journal articleBousquet J, Sousa-Pinto B, Vieira RJ, et al., 2026,
Methodology for the Development of the Allergic Rhinitis and Its Impact on Asthma (ARIA)-EAACI 2024-2025 Guidelines: From Evidence-to-Decision Frameworks to Digitalised Shared Decision-Making Algorithms.
, Allergy, Vol: 81, Pages: 427-453The Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines produced their first edition in 1999, with subsequent revisions in 2008, 2010, 2016 and 2019. A new iteration of ARIA-ARIA 2024-2025-in collaboration with EAACI is currently being developed, focusing on the management of allergic rhinitis. ARIA 2024-2025 follows the GRADE framework and is endorsed by the European Academy of Allergy and Clinical Immunology (EAACI). A set of approaches has been used to develop guideline questions, including surveying key opinion leaders and using artificial intelligence (AI)-based tools to analyse web searches on allergic rhinitis and to generate questions. Each prioritised guideline question is assessed through an Evidence-to-Decision (EtD) framework. EtDs support the systematic and transparent formulation of recommendations, comprising 12 criteria for which the best available evidence should be sought. In the context of ARIA-EAACI 2024-2025, such evidence is derived not only from randomised controlled trials but also-among others-from patient-generated data sources that better reflect the affected individuals' perspectives. Moreover, ARIA-EAACI 2024-2025 incorporates evidence on planetary health. Developed guideline recommendations will support the creation of digitalised decision algorithms and care pathways. This paper describes the methodology used to develop the person-centred, digitally enabled and AI-assisted ARIA-EAACI 2024-2025. Among others, it describes (i) the development and prioritisation of guideline questions, (ii) sources of evidence for EtDs and (iii) the development of digitalised decision algorithms and care pathways.
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Journal articleKong E, Cucco A, Custovic A, et al., 2026,
Machine learning in allergy research: A bibliometric review
, IMMUNOLOGY LETTERS, Vol: 277, ISSN: 0165-2478 -
Journal articleShamji MH, Boyle RJ, 2026,
Advancing Allergy Research Through Innovative Methodologies and Epithelial Immunology.
, Clin Exp Allergy, Vol: 56, Pages: 121-123 -
Journal articleWilson-Morkeh H, Seluk L, Bosch P, et al., 2026,
Targeting Immunologic Pathways in Eosinophilic Granulomatosis With Polyangiitis: Translating Emerging Evidence Into Clinical Practice.
, AllergyEosinophilic granulomatosis with polyangiitis (EGPA) is a rare and potentially life-threatening systemic, inflammatory disease with multi-organ manifestations, variable presentation and complex pathology. Multiple interconnected immunological pathways are implicated in EGPA pathology, including a type-2 immune response driving predominantly eosinophilic inflammation, B-cell mediated autoimmunity, neutrophil activation, and the generation of pathogenic anti-neutrophil cytoplasmic antibodies, all of which can contribute to tissue/organ damage. High-dose glucocorticoids are the mainstay treatment for EGPA, but over the past two decades the development of biologic treatments targeting interleukin (IL)-5, eosinophils and B-cells has revitalized the treatment landscape. Mepolizumab, a humanized monoclonal antibody that specifically targets IL-5, and benralizumab, which targets the IL-5 receptor (IL-5Rα), are both approved for the treatment of patients with non-severe relapsing or refractory EGPA. In Phase III trials, these biologics have demonstrated favorable safety profiles and efficacy, with treatment leading to remission induction, remission maintenance, and oral glucocorticoid sparing benefits. However, as understanding of the full complexity of EGPA pathogenesis improves, new treatment targets are emerging. Consequently, understanding key pathogenic mechanisms at the patient level, enabling a more tailored treatment approach, is an important goal for future research.
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Journal articleStölting H, Raftery AL, Walker SA, et al., 2026,
Epidermal growth factor receptor controls sex differences in lung type 2 responses to inhaled allergen.
, Sci Immunol, Vol: 11Hormonal disruptions are associated with poor asthma control in females, yet how these phenomena are linked remains unknown. Here, we investigated distinct allergen-induced immune responses between the sexes during maturation. By 6 weeks of life, female mice exposed to the aeroallergen house dust mite (HDM) from postnatal day 7 exhibited stronger type 2 (T2) immune responses and higher lung interleukin-33 (IL-33) than males. IL-33 administration to HDM-sensitized males was sufficient to augment T2 immunity and up-regulated epidermal growth factor receptor (EGFR) on T helper 2 (TH2) cells. EGFR inhibition abrogated T2 cytokine production in vitro. In vivo, EGFR inhibition reduced T2 immunity in females only, thereby abolishing any sex differences. 17β-estradiol (E2) heightened lung Il33 expression and T2 responses of HDM-sensitized males, akin to levels in females. EGFR's ability to drive sex differences in lung T2 responses downstream of E2 and IL-33 may link hormonal disruptions to poor asthma control.
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Journal articleCucco A, Simpson A, Murray C, et al., 2026,
Clustering lung function and symptom profiles for asthma risk stratification
, Scientific Reports, Vol: 16, ISSN: 2045-2322Asthma is a heterogeneous condition often studied through wheeze alone, yet the interplay between lung function and reported symptoms remains underexplored. To capture this heterogeneity, we applied Bayesian Profile Regression to data from school-age children in two prospective birth cohorts, integrating airway hyperresponsiveness, lung function, bronchodilator reversibility, allergic sensitisation, reported symptoms, and physician diagnosis. In the Manchester Allergy and Asthma Study (discovery cohort), five reproducible clusters were identified: HA-LLF (high asthma-low lung function), HA-NLF (high asthma-near-normal lung function), LA-LLF (low asthma-low lung function), LA-NLF (low asthma-normal lung function), and INT-SYM (intermediate asthma with prominent symptoms). The HA-LLF and HA-NLF clusters had very high asthma prevalence (80–100%), but differed markedly in lung function, airway responsiveness, bronchodilator reversibility, sensitisation, and symptom burden. The LA-HLF and LA-NLF clusters with low asthma prevalence (<5%) displayed contrasting lung function profiles, while INT-SYM (~50% asthma prevalence) was largely defined by prominent symptoms such as chest tightness and shortness of breath. These subtypes were replicated in an independent cohort, Isle of Wight. Our findings demonstrate that integrating physiological, immunological, and symptom-based measures yields clinically meaningful asthma subtypes beyond wheeze-based definitions and may support more precise disease classification.
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Journal articleBush A, 2026,
Back to the Mucus: Introduction to an <i>AJRCCM</i> Special Section on Airway Mucus
, American Journal of Respiratory and Critical Care Medicine, ISSN: 1073-449X -
Journal articleMolyneaux PL, Mogulkoc N, Gunen H, et al., 2026,
Oral Nalbuphine in Idiopathic Pulmonary Fibrosis-Associated Cough: The CORAL Randomized Clinical Trial.
, JAMAIMPORTANCE: For patients with idiopathic pulmonary fibrosis (IPF), cough impairs quality of life; effective treatments for IPF-associated cough are needed. OBJECTIVE: To determine if nalbuphine extended release (ER), a κ opioid receptor agonist and μ-opioid receptor antagonist, decreases cough compared with placebo in patients with IPF-associated cough. DESIGN, SETTING, AND PARTICIPANTS: In this randomized, double-blind, placebo-controlled phase 2b trial conducted at 52 sites in 10 countries, patients with IPF, chronic cough for at least 8 weeks, and a Cough Severity Numerical Rating Scale (0, no cough; 10, worst possible cough) score of 4 or higher were enrolled from February 2024 to February 2025, with last follow-up in April 2025. Statistical analyses were conducted from May to August 2025. INTERVENTION: Patients were randomized 1:1:1:1 to receive nalbuphine ER at doses of 27 mg, 54 mg, or 108 mg or placebo twice daily for 6 weeks. MAIN OUTCOMES AND MEASURES: The primary outcome was the relative change from baseline in 24-hour cough frequency (coughs/h), measured with a digital cough monitor, for nalbuphine ER compared with placebo at week 6. The key secondary outcome was the relative change from baseline in the patient-reported cough frequency (Evaluating Respiratory Symptoms in IPF cough subscale; scores range from 0-4, lower scores indicate lesser cough frequency) at week 6. RESULTS: Of the 223 patients screened, 165 were randomized (42, 43, 40, and 40 to receive nalbuphine ER 27 mg, 54 mg, and 108 mg, and placebo, respectively) and 160 were included in the primary analysis (median age, 71 [range, 51-85] years; 28.5% female). The baseline mean (SD) cough count was 28.3 (27.4) coughs/h. In the nalbuphine ER 27 mg, 54 mg, and 108 mg twice-daily groups, the mean relative decrease in the cough count and the absolute decrease in coughs/h were 47.9% (from 24.6 to 11.9; P = .008), 53.4% (from 28.0 to 14.9; P < .001), and 60.2%
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Journal articleKhan F, Stewart I, Howard L, et al., 2026,
Comprehensive characterisation of individuals with fibrotic interstitial lung disease: baseline insights from the INJUSTIS study.
, BMJ Open Respir Res, Vol: 13BACKGROUND: Interstitial lung disease (ILD) represents a group of complex parenchymal conditions characterised by varying clinical trajectories. The It's Not JUST Idiopathic Pulmonary Fibrosis Study seeks to identify genetic, proteomic and clinical biomarkers that distinguish rapidly progressive fibrotic phenotypes from stable phenotypes irrespective of aetiology. This manuscript presents baseline insights from the recruited cohort. METHODS: In this prospective, longitudinal study, participants with fibrotic ILDs, including idiopathic pulmonary fibrosis (IPF), fibrotic hypersensitivity pneumonitis, rheumatoid arthritis-associated ILD, asbestosis and unclassifiable ILD, were enrolled from 24 UK sites. Participants underwent comprehensive baseline evaluation including demographics, exposure history, lung function testing, 6-min walk tests, blood sampling and standardised questionnaires to assess symptoms and quality of life. RESULTS: A total of 272 participants were recruited, predominantly older white males with a smoking history. Baseline lung function showed comparable forced vital capacity (mean 89.0% predicted), diffusion of carbon monoxide (mean 57.9% predicted) and 6-min walk distance (mean 302 m) across ILD subtypes. Hypertension was the most prevalent comorbidity, affecting 40.8% of participants, with no significant differences across subtypes. Anxiety and depression were notably lower in IPF than non-IPF (4.5%; 21.0%). Previous occupational exposure was reported in 68.8% of participants, with asbestos exposure the most prevalent (36%). Bird exposure was reported by 40.4% of participants, with no significant differences across subtypes. No significant differences in health-related quality of life scores were observed across subtypes. CONCLUSIONS: Despite varied aetiologies, fibrotic ILDs exhibit demographic and functional similarities, including lung function and health-related quality of life suggesting commonalities in disease mechanisms. TRIAL REGISTRATION
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Journal articleRowbotham NJ, Jeanpierre M, Bush A, et al., 2026,
New pathogenic PTPN2 variant leading to childhood interstitial lung disease.
, ThoraxProtein tyrosine phosphatase non-receptor type 2 (PTPN2) is a tyrosine phosphatase involved in T cell receptor signal transduction and cytokine response. Loss of function variants have previously been linked with immune mediated diseases such as inflammatory bowel disorders, rheumatoid arthritis and type 1 diabetes. We present a case of childhood interstitial lung disease with a newly identified pathogenic (PTPN2) gene variant in a boy aged 4 years.
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Journal articleRidd MJ, Brown SJ, Beattie P, et al., 2026,
Reply to Comment on 'Food Allergy Test-Guided Dietary Advice for Children With Atopic Dermatitis: A Consensus Study'.
, Pediatr Dermatol -
Journal articleKarp T, Merid SK, Kermani NZ, et al., 2026,
Nasal gene expression shows a distinct signature in type 2-high asthma but not in type 2-low disease.
, J Allergy Clin ImmunolBACKGROUND: Type 2 (T2)-low asthma is defined by low levels of T2 inflammation and is associated with resistance to inhaled corticosteroids. Its molecular mechanisms are mostly unknown, and treatment options are limited. We previously showed that nasal brush transcriptomes differ between asthma and controls, reflecting disease-relevant biology. OBJECTIVE: We explored nasal gene expression related to T2-low asthma in the ATLANTIS cohort. METHODS: We compared nasal brush RNA sequencing data between 82 T2-low and 63 T2-high asthma patients and 57 controls. T2-low asthma was defined as blood eosinophil counts < 0.15 × 109/L and Feno < 25 ppb and T2-high as blood eosinophil counts > 0.3 × 109/L and Feno > 25 ppb. Weighted gene coexpression network analysis (WGCNA) was applied to identify gene modules associated with T2-low asthma. The BAMSE and U-BIOPRED cohorts were used for replication analyses. RESULTS: Although differentially expressed genes were found in patients with T2-high asthma across all 3 cohorts, no differentially expressed genes were observed in individuals with T2-low disease compared to controls in ATLANTIS, nor consistently across other cohorts. Our assessment of molecular heterogeneity could not attribute this result to greater intersample variability within the T2-low group. WGCNA in ATLANTIS identified "black" and "purple" gene modules linked to T2-low asthma, with genes enriched in T-cell immunity and ribosomal RNA biology pathways, respectively. The "black" module was replicated in U-BIOPRED and showed the same direction in BAMSE. CONCLUSION: T2-high asthma shows a distinct nasal gene expression signature compared to healthy controls, while patients with T2-low asthma exhibit no consistent changes. Future studies should explore T-cell immunity in T2-low asthma and integrate lower airway multiomics data.
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