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A Novel Alpaca-Derived Polyclonal Antibody Enables Highly Sensitive Detection of Gliadin in Food. 一种新的羊驼源性多克隆抗体用于食品中麦胶蛋白的高灵敏度检测。
IF 12 1区 医学 Q1 ALLERGY Pub Date : 2026-02-09 DOI: 10.1111/all.70255
Ruyu Fang, Jing Yang, Yifan Liang, Jiarui Pang, Yupeng Zhao, Xiangpeng Han, Yu Wang, Zhenlin Xu, Hong Wang
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引用次数: 0
Tissue-Serum Metabolomics Identifies Lipid Signatures in Eosinophilic Chronic Rhinosinusitis. 组织-血清代谢组学鉴定嗜酸性慢性鼻窦炎的脂质特征。
IF 12 1区 医学 Q1 ALLERGY Pub Date : 2026-02-07 DOI: 10.1111/all.70239
Yibo Liang, Zhili Li, Chenting Zhang, Jiarui Liu, Kai Zhang, Guimin Zhang
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引用次数: 0
Update on Non-Biological and RNA-Based Therapeutics in Chronic Inflammatory Diseases: Precision Medicine Through Small Molecules. 慢性炎症疾病的非生物和rna治疗进展:小分子精准医学
IF 12 1区 医学 Q1 ALLERGY Pub Date : 2026-02-07 DOI: 10.1111/all.70235
F Roth-Walter, I M Adcock, C Benito-Villalvilla, R Bianchini, L Bjermer, G Caramori, L Cari, K F Chung, Z Diamant, I Eguiluz-Gracia, E F Knol, M Jesenak, F Levi-Schaffer, G Nocentini, L O'Mahony, O Palomares, F Redegeld, M Sokolowska, B Van Esch, M Zurlo, C Stellato

In the last decades, critical advancements in research technology and knowledge on disease mechanisms steered therapeutic approaches for chronic inflammatory diseases towards unprecedented target specificity. For allergic and chronic lung diseases, biologic drugs pioneered this goal, acquiring on the way-through the clinical use of monoclonal antibodies-a deeper understanding of how inflammatory and immune pathways are configured in disease-specific patterns. In this biomarker-driven approach, synthetic small molecule drugs (SMDs) were perceived as lagging behind in innovation for their relative lack of specificity. This was, however, mostly due to a shift in focus towards biologics rather than true obsolescence of SMDs. In the same timeframe, in fact, advances in structural biology and medicinal chemistry, bioinformatics and artificial intelligence held steadily SMDs' innovation and relevance. The use of kinase inhibitors, well established in the treatment of cancer and rheumatological diseases, is now approved for some allergic skin diseases and is approaching asthma and COPD with several clinical trials; moreover, new therapeutics targeting mast cell receptors and molecules involved in innate immunity are entering preclinical and clinical testing. Alongside, the portfolio of biologics is harboring the expansion of RNA therapeutics, which gained global recognition during the COVID-19 pandemic due to RNA vaccines. Different types of RNA therapeutics, including those based on different non-coding RNAs, are advancing to agency approval and market, thanks to improvements in molecule stability and delivery systems. In summary, the evidence presented in this position paper illustrates that precision medicine is becoming a goal shared between synthetic SMDs and biologics, both protein/antibody-based and RNA therapeutics. We review the current state, unmet needs and opportunities within this evolving landscape, highlighting how small molecular species, both synthetic as SMDs and biologic in nature as RNA, can contribute to the precision medicine approach along with protein and antibody-based biologics and cell therapies.

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引用次数: 0
The International Guideline for the Definition, Classification, Diagnosis and Management of Urticaria 《国际荨麻疹定义、分类、诊断和治疗指南》
IF 12.4 1区 医学 Q1 ALLERGY Pub Date : 2026-02-06 DOI: 10.1111/all.70210
T. Zuberbier, Z. Abdul Hameed Ansari, A. H. Abdul Latiff, M. M. Abuzakouk, M. S. Agcaoili‐De Jesus, R. C. Agondi, M. Al‐Ahmad, A. A. Alangari, H. Alhameli, C. D. Alonso Bello, S. Alshareef, S. Al‐Tamemi, S. Altrichter, H. Al Wahshi, S. Aquilina, M. Araújo, R. Arnaout, R. Asero, B. Ballmer‐Weber, C. Bangert, A. Bauer, M. Ben‐Shoshan, J. Bernstein, C. Bindslev‐Jensen, M. Bizjak, I. Boccon‐Gibod, H. Bonnekoh, L. Bouillet, K. Brockow, Z. Brzoza, M. Bulatović Ćalasan, A. Bulkhi, T. Buttgereit, A. Bygum, T. Caballero, O. Calderon, R. Campos, M. Cancian, E. Carne, M. A. Castor, I. Cerecedo, T. Çetinarslan, I. Cherrez‐Ojeda, N. Chkhikvadze, H. J. Chong‐Neto, K. Choo, G. Christoff, C.‐Y. Chu, K. Ciupka, N. Conlon, C. Costa, T. Craig, P. Criado, I. Danilycheva, R. Darlenski, E. De Arruda Chaves, L. de Montjoye, M. S. Doutre, A. Du‐Thanh, D. Ebo, S. Elkhalifa, S. Elmariah, T. El‐Shanawany, L. F. Ensina, R. Ertaş, R. Fachini Jardim Criado, M. Ferrer, S. Ferrucci, J. S. Fok, D. Fomina, L. Fonacier, G. Fouda, I. Francescantonio, A. Fukunaga, C. A. Galvan Calle, E. Garcia, K. Gáspár, A. Gelincik, S. Geng, K. Godse, M. Gonçalo, M. Gotua, C. Grattan, M. Grosber, G. Guidos Fogelbach, M. Guilarte, R. Guillod, E. Hamelmann, J. Hawkes, K. Hayama, R. Heuer, M. Hide, W. Hoetzenecker, N. Inomata, H.‐R. Kang, A. Kaplan, A. Kapp, M. Karam, A. Kasperska‐Zajac, C. H. Katelaris, A. Kessel, M. Khoshkhui, B. Kim, T. Kinaciyan, E. Kocatürk, M. Kolacinska‐Flont, P. Kolkhir, G. N. Konstantinou, M. Kosnik, D. Krasowska, K. Kulthanan, M. S. Kumaran, I. Kuprys‐Lipinska, M. Labrador, J. I. Larco, D. Larenas‐Linnemann, E. Latysheva, E. Lazaridou, P. H. Li, H. Lima, U. Lippert, M. Magerl, M. Makris, J. Alves Marcelino, A. V. Marzano, I. Medina, R. Meshkova, D. Micallef, R. Mohammed Ali, C. G. Mortz, M. Munoz, H. N. G. Oude Elberink, A. Nakonechna, I. Nasr, A. Nast, E. Netchiporouk, E. Nettis, S. Nieto, I. Ogueta Canales, T.‐L. Okas, R. L. Orfali, E. Özkaya, C. Parisi, A. Pennitz, R. Pawankar, M. P. Pereira, J. Peter, E. Petkova, P. D. Pigatto, I. Podder, T. Popov, G. Porebski, P. Pyatilova, G. D. Ramon, H. A. Ratti Sisa, M. Recto, K. Ress, K. Ridge, M. Riedl, C. Ritchie, N. Rosario Filho, I. Rosmaninho, M. Rudenko, M. Rukhadze, K. Rutkowski, V. Sabato, U. M. Sahiner, S. Saini, F. Saleh Al Sabbagh, A. Salman, F. Salvo, J. Sanchez, A. Santucci, S. Schliemann, P. Schmid‐Grendelmeier, B. E. Sekerel, F. Serpa, F. Sheikh, J. Sheikh, H. Shendi, F. Siebenhaar, M. Sonomjamts, A. Soria, B. Sousa Pinto, M. Staevska, P. Staubach, M. Stephan, K. Stevanovic, L. Stingeni, M. Stobiecki, Ö. Su Küçük, G. Sussman, A. Szegedi, S. Takahagi, A. Tanaka, N. Teovska Mitrevska, S. F. Thomsen, E. Toubi, F. Tsatsou, M. Turk, Z. Vadasz, A. Valerieva, S. Valle, M. v. Doorn, B. Veleiro Perez, C. E. Vera Ayala, C. Vestergaard, R. J. Vieira, C. W. Maruta, B. Wedi, R. N. Werner, E. W. Y. Yap, P. Xepapadaki, Y. Xiang, Y.‐M. Ye, P. Yong, G. Yosipovitch, A. Z. J. Zalewska‐Janowska, C. Zeyen, Z. Zhao, M. Metz, A. M. Giménez‐Arnau
This update and revision of the international guideline for urticaria was developed in accordance with the methods recommended by Cochrane and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. It is an initiative of the Global Allergy and Asthma Excellence Network (GA 2 LEN) and its Urticaria and Angioedema Centers of Reference and Excellence (UCAREs and ACAREs), with the participation of 210 delegates from 107 national and international societies, from 59 countries. The consensus conference was held on December 6th, 2024. This guideline was acknowledged and accepted by the European Union of Medical Specialists (UEMS). Urticaria is a frequent, mast cell‐driven disease, defined by a rapid appearance of wheals, angioedema, or both. The lifetime prevalence of acute urticaria is estimated to be approximately 20%. Chronic urticaria, categorized as either chronic spontaneous urticaria or chronic inducible urticaria, is disabling, impairs quality of life, and affects performance at work and school, however, novel therapies are available. This updated version of the international guideline for urticaria covers the definition and classification of urticaria and outlines expert‐guided and evidence‐based diagnostic and therapeutic approaches for the different subtypes of urticaria.
{"title":"The International Guideline for the Definition, Classification, Diagnosis and Management of Urticaria","authors":"T. Zuberbier, Z. Abdul Hameed Ansari, A. H. Abdul Latiff, M. M. Abuzakouk, M. S. Agcaoili‐De Jesus, R. C. Agondi, M. Al‐Ahmad, A. A. Alangari, H. Alhameli, C. D. Alonso Bello, S. Alshareef, S. Al‐Tamemi, S. Altrichter, H. Al Wahshi, S. Aquilina, M. Araújo, R. Arnaout, R. Asero, B. Ballmer‐Weber, C. Bangert, A. Bauer, M. Ben‐Shoshan, J. Bernstein, C. Bindslev‐Jensen, M. Bizjak, I. Boccon‐Gibod, H. Bonnekoh, L. Bouillet, K. Brockow, Z. Brzoza, M. Bulatović Ćalasan, A. Bulkhi, T. Buttgereit, A. Bygum, T. Caballero, O. Calderon, R. Campos, M. Cancian, E. Carne, M. A. Castor, I. Cerecedo, T. Çetinarslan, I. Cherrez‐Ojeda, N. Chkhikvadze, H. J. Chong‐Neto, K. Choo, G. Christoff, C.‐Y. Chu, K. Ciupka, N. Conlon, C. Costa, T. Craig, P. Criado, I. Danilycheva, R. Darlenski, E. De Arruda Chaves, L. de Montjoye, M. S. Doutre, A. Du‐Thanh, D. Ebo, S. Elkhalifa, S. Elmariah, T. El‐Shanawany, L. F. Ensina, R. Ertaş, R. Fachini Jardim Criado, M. Ferrer, S. Ferrucci, J. S. Fok, D. Fomina, L. Fonacier, G. Fouda, I. Francescantonio, A. Fukunaga, C. A. Galvan Calle, E. Garcia, K. Gáspár, A. Gelincik, S. Geng, K. Godse, M. Gonçalo, M. Gotua, C. Grattan, M. Grosber, G. Guidos Fogelbach, M. Guilarte, R. Guillod, E. Hamelmann, J. Hawkes, K. Hayama, R. Heuer, M. Hide, W. Hoetzenecker, N. Inomata, H.‐R. Kang, A. Kaplan, A. Kapp, M. Karam, A. Kasperska‐Zajac, C. H. Katelaris, A. Kessel, M. Khoshkhui, B. Kim, T. Kinaciyan, E. Kocatürk, M. Kolacinska‐Flont, P. Kolkhir, G. N. Konstantinou, M. Kosnik, D. Krasowska, K. Kulthanan, M. S. Kumaran, I. Kuprys‐Lipinska, M. Labrador, J. I. Larco, D. Larenas‐Linnemann, E. Latysheva, E. Lazaridou, P. H. Li, H. Lima, U. Lippert, M. Magerl, M. Makris, J. Alves Marcelino, A. V. Marzano, I. Medina, R. Meshkova, D. Micallef, R. Mohammed Ali, C. G. Mortz, M. Munoz, H. N. G. Oude Elberink, A. Nakonechna, I. Nasr, A. Nast, E. Netchiporouk, E. Nettis, S. Nieto, I. Ogueta Canales, T.‐L. Okas, R. L. Orfali, E. Özkaya, C. Parisi, A. Pennitz, R. Pawankar, M. P. Pereira, J. Peter, E. Petkova, P. D. Pigatto, I. Podder, T. Popov, G. Porebski, P. Pyatilova, G. D. Ramon, H. A. Ratti Sisa, M. Recto, K. Ress, K. Ridge, M. Riedl, C. Ritchie, N. Rosario Filho, I. Rosmaninho, M. Rudenko, M. Rukhadze, K. Rutkowski, V. Sabato, U. M. Sahiner, S. Saini, F. Saleh Al Sabbagh, A. Salman, F. Salvo, J. Sanchez, A. Santucci, S. Schliemann, P. Schmid‐Grendelmeier, B. E. Sekerel, F. Serpa, F. Sheikh, J. Sheikh, H. Shendi, F. Siebenhaar, M. Sonomjamts, A. Soria, B. Sousa Pinto, M. Staevska, P. Staubach, M. Stephan, K. Stevanovic, L. Stingeni, M. Stobiecki, Ö. Su Küçük, G. Sussman, A. Szegedi, S. Takahagi, A. Tanaka, N. Teovska Mitrevska, S. F. Thomsen, E. Toubi, F. Tsatsou, M. Turk, Z. Vadasz, A. Valerieva, S. Valle, M. v. Doorn, B. Veleiro Perez, C. E. Vera Ayala, C. Vestergaard, R. J. Vieira, C. W. Maruta, B. Wedi, R. N. Werner, E. W. Y. Yap, P. Xepapadaki, Y. Xiang, Y.‐M. Ye, P. Yong, G. Yosipovitch, A. Z. J. Zalewska‐Janowska, C. Zeyen, Z. Zhao, M. Metz, A. M. Giménez‐Arnau","doi":"10.1111/all.70210","DOIUrl":"https://doi.org/10.1111/all.70210","url":null,"abstract":"This update and revision of the international guideline for urticaria was developed in accordance with the methods recommended by Cochrane and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. It is an initiative of the Global Allergy and Asthma Excellence Network (GA <jats:sup>2</jats:sup> LEN) and its Urticaria and Angioedema Centers of Reference and Excellence (UCAREs and ACAREs), with the participation of 210 delegates from 107 national and international societies, from 59 countries. The consensus conference was held on December 6th, 2024. This guideline was acknowledged and accepted by the European Union of Medical Specialists (UEMS). Urticaria is a frequent, mast cell‐driven disease, defined by a rapid appearance of wheals, angioedema, or both. The lifetime prevalence of acute urticaria is estimated to be approximately 20%. Chronic urticaria, categorized as either chronic spontaneous urticaria or chronic inducible urticaria, is disabling, impairs quality of life, and affects performance at work and school, however, novel therapies are available. This updated version of the international guideline for urticaria covers the definition and classification of urticaria and outlines expert‐guided and evidence‐based diagnostic and therapeutic approaches for the different subtypes of urticaria.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"177 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146129374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Laundry Detergents Enhance Sensitization to Co-Inhaled Allergens and Exacerbate Airway Inflammation in Mice. 洗衣剂增强小鼠对共同吸入过敏原的致敏性并加剧气道炎症。
IF 12 1区 医学 Q1 ALLERGY Pub Date : 2026-02-05 DOI: 10.1111/all.70245
Naoko Nagano, Masato Tamari, Hiromichi Yamamoto, Hisataka Nakazaki, Satoshi Fujita, Yuka Hayashi, Kenichiro Motomura, Sanne Johanna Maria de Bruijn, Ken Arae, Terufumi Kubo, Masashi Ikutani, Katsuko Sudo, Hidenori Kage, Hirohisa Saito, Susumu Nakae, Kenji Matsumoto, Cezmi A Akdis, Hideaki Morita

Background: Our previous study demonstrated that laundry detergents induce group 2 innate lymphoid cell-driven eosinophilic airway inflammation by disrupting airway epithelial barriers and promoting IL-33 release, and that detergent residues are present in nearly all household dust. However, their impact on allergen-induced airway inflammation remains unclear.

Methods: C57BL/6 background mice were intranasally primed four times with ovalbumin (OVA) or house dust mite (HDM) allergens in the presence or absence of a commercial laundry detergent. Following priming, mice were challenged with the same antigen for 3 consecutive days and sacrificed the day after the final challenge. Bronchoalveolar lavage fluid (BALF) and sera were analyzed by ELISA. Lungs were evaluated histologically and analyzed by qPCR.

Results: Mice intranasally primed with antigen in the presence of detergent exhibited eosinophilic airway inflammation upon antigen challenge, accompanied by increased IL-5 and IL-13 levels in the BALF. Intranasal administration of detergent and antigen also stimulated antigen-specific IgE production. These detergent- and allergen-induced type 2 responses were significantly suppressed in Il33-/- and Il13-/- mice. Administration of an anti-IL-4 receptor α chain antibody during the challenge phase reduced eosinophil counts in the BALF and antigen-specific IgE levels in the serum. By contrast, anti-IL-33 antibody treatment during the challenge phase did not affect eosinophilic airway inflammation or antigen-specific IgE production.

Conclusions: Laundry detergents promote sensitization to co-inhaled allergens and exacerbate eosinophilic airway inflammation and antigen-specific IgE responses via IL-33 and IL-13. These findings suggest that detergents can act as adjuvants that facilitate airway sensitization.

背景:我们之前的研究表明,洗涤剂通过破坏气道上皮屏障和促进IL-33的释放,诱导2组先天淋巴细胞驱动的嗜酸性气道炎症,并且洗涤剂残留物几乎存在于所有的家庭灰尘中。然而,它们对过敏原诱导的气道炎症的影响尚不清楚。方法:C57BL/6背景小鼠在有或没有商业洗衣液的情况下,鼻内注入四次卵白蛋白(OVA)或屋尘螨(HDM)过敏原。启动后,连续3天用相同的抗原刺激小鼠,最后一次刺激后第1天处死。ELISA法检测支气管肺泡灌洗液(BALF)及血清。采用qPCR对肺进行组织学评估和分析。结果:在洗涤剂存在的情况下,经鼻内注入抗原的小鼠在抗原刺激下表现出嗜酸性气道炎症,并伴有BALF中IL-5和IL-13水平升高。鼻内给药洗涤剂和抗原也刺激了抗原特异性IgE的产生。这些洗涤剂和过敏原诱导的2型反应在Il33-/-和Il13-/-小鼠中被显著抑制。在攻毒期给予抗il -4受体α链抗体可降低血清中BALF中的嗜酸性粒细胞计数和抗原特异性IgE水平。相比之下,在攻毒阶段抗il -33抗体治疗不影响嗜酸性气道炎症或抗原特异性IgE的产生。结论:洗衣粉通过IL-33和IL-13促进对共同吸入过敏原的致敏,加剧嗜酸性气道炎症和抗原特异性IgE反应。这些发现表明,洗涤剂可以作为辅助剂,促进气道致敏。
{"title":"Laundry Detergents Enhance Sensitization to Co-Inhaled Allergens and Exacerbate Airway Inflammation in Mice.","authors":"Naoko Nagano, Masato Tamari, Hiromichi Yamamoto, Hisataka Nakazaki, Satoshi Fujita, Yuka Hayashi, Kenichiro Motomura, Sanne Johanna Maria de Bruijn, Ken Arae, Terufumi Kubo, Masashi Ikutani, Katsuko Sudo, Hidenori Kage, Hirohisa Saito, Susumu Nakae, Kenji Matsumoto, Cezmi A Akdis, Hideaki Morita","doi":"10.1111/all.70245","DOIUrl":"https://doi.org/10.1111/all.70245","url":null,"abstract":"<p><strong>Background: </strong>Our previous study demonstrated that laundry detergents induce group 2 innate lymphoid cell-driven eosinophilic airway inflammation by disrupting airway epithelial barriers and promoting IL-33 release, and that detergent residues are present in nearly all household dust. However, their impact on allergen-induced airway inflammation remains unclear.</p><p><strong>Methods: </strong>C57BL/6 background mice were intranasally primed four times with ovalbumin (OVA) or house dust mite (HDM) allergens in the presence or absence of a commercial laundry detergent. Following priming, mice were challenged with the same antigen for 3 consecutive days and sacrificed the day after the final challenge. Bronchoalveolar lavage fluid (BALF) and sera were analyzed by ELISA. Lungs were evaluated histologically and analyzed by qPCR.</p><p><strong>Results: </strong>Mice intranasally primed with antigen in the presence of detergent exhibited eosinophilic airway inflammation upon antigen challenge, accompanied by increased IL-5 and IL-13 levels in the BALF. Intranasal administration of detergent and antigen also stimulated antigen-specific IgE production. These detergent- and allergen-induced type 2 responses were significantly suppressed in Il33<sup>-/-</sup> and Il13<sup>-/-</sup> mice. Administration of an anti-IL-4 receptor α chain antibody during the challenge phase reduced eosinophil counts in the BALF and antigen-specific IgE levels in the serum. By contrast, anti-IL-33 antibody treatment during the challenge phase did not affect eosinophilic airway inflammation or antigen-specific IgE production.</p><p><strong>Conclusions: </strong>Laundry detergents promote sensitization to co-inhaled allergens and exacerbate eosinophilic airway inflammation and antigen-specific IgE responses via IL-33 and IL-13. These findings suggest that detergents can act as adjuvants that facilitate airway sensitization.</p>","PeriodicalId":122,"journal":{"name":"Allergy","volume":" ","pages":""},"PeriodicalIF":12.0,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Comorbid Chronic Rhinosinusitis and Asthma: Shared Risk Factors and Treatment Implications-An EAACI Task Force Report. 慢性鼻窦炎和哮喘共病:共同的危险因素和治疗意义——EAACI工作组报告。
IF 12 1区 医学 Q1 ALLERGY Pub Date : 2026-02-05 DOI: 10.1111/all.70237
Sanna Toppila-Salmi, Sietze Reitsma, Valérie Hox, Simon Gane, Philippe Gevaert, Juan Maza-Solano, Alma Helevä, Ida Sulku, Kaisa Santala, Iiris Kangasniemi, Ludger Klimek, Adam Chaker, Aspasia Karavelia, Michael Rudenko, Oliver Pfaar, Laura Van Gerven, Shaari Ariana, Michele Schiappoli, Marie Lundberg, Jan Hagemann, Ibon Eguíluz-Gracia, Andre Moreira

Chronic rhinosinusitis (CRS) and asthma are prevalent conditions that often coexist. These diseases share common inflammatory mechanisms, such as T-helper cell 2 (T2)-high inflammation, driven by interleukin (IL)-4, IL-5, and IL-13 cytokines. The frequent comorbidity between CRS, especially CRS with nasal polyps (CRSwNP), and asthma exacerbates disease severity, impairs quality of life, and complicates treatment. Patients with NSAID-exacerbated respiratory disease (N-ERD) represent a severe phenotype of this disease, characterized by the coexistence of CRSwNP, asthma, and NSAID hypersensitivity, which poses unique therapeutic challenges. This EAACI Task Force explores the shared risk factors, including genetic predispositions, epithelial barrier dysfunction, microbiome dysbiosis, underlying CRS, and asthma. It also evaluates current therapeutic strategies such as biologics, aspirin therapy after desensitization (ATAD), and endoscopic sinus surgery (ESS). Biologics have shown their effectiveness and safety in the treatment of asthma and CRS. Dupilumab, mepolizumab, depemokimab, and omalizumab have emerged as transformative therapies, particularly for patients with severe type 2 inflammation. Tezepelulumab is effective for both T2-high and T2-low asthma and CRSwNP. Itepekimab has shown its effect in asthma and is under investigation for CRSwNP. Omalizumab is effective in allergic asthma and CRSwNP. ATAD provides an additional disease-modifying approach for N-ERD, though patient adherence and tolerability remain critical challenges. ESS significantly improves asthma control, reduces medication use, and enhances sinonasal outcomes, particularly in severe asthma cases; however, these patients often need recurring surgeries. Despite these advances, treatment outcomes vary based on individual phenotypes and endotypes, underscoring the need for personalized approaches. The report highlights gaps in the literature, such as the lack of head-to-head trials comparing biologics, ATAD, and surgery. Future research should focus on refining treatment algorithms, identifying biomarkers for treatment selection, and assessing long-term outcomes to optimize care for patients with CRS, asthma, and N-ERD.

{"title":"Comorbid Chronic Rhinosinusitis and Asthma: Shared Risk Factors and Treatment Implications-An EAACI Task Force Report.","authors":"Sanna Toppila-Salmi, Sietze Reitsma, Valérie Hox, Simon Gane, Philippe Gevaert, Juan Maza-Solano, Alma Helevä, Ida Sulku, Kaisa Santala, Iiris Kangasniemi, Ludger Klimek, Adam Chaker, Aspasia Karavelia, Michael Rudenko, Oliver Pfaar, Laura Van Gerven, Shaari Ariana, Michele Schiappoli, Marie Lundberg, Jan Hagemann, Ibon Eguíluz-Gracia, Andre Moreira","doi":"10.1111/all.70237","DOIUrl":"https://doi.org/10.1111/all.70237","url":null,"abstract":"<p><p>Chronic rhinosinusitis (CRS) and asthma are prevalent conditions that often coexist. These diseases share common inflammatory mechanisms, such as T-helper cell 2 (T2)-high inflammation, driven by interleukin (IL)-4, IL-5, and IL-13 cytokines. The frequent comorbidity between CRS, especially CRS with nasal polyps (CRSwNP), and asthma exacerbates disease severity, impairs quality of life, and complicates treatment. Patients with NSAID-exacerbated respiratory disease (N-ERD) represent a severe phenotype of this disease, characterized by the coexistence of CRSwNP, asthma, and NSAID hypersensitivity, which poses unique therapeutic challenges. This EAACI Task Force explores the shared risk factors, including genetic predispositions, epithelial barrier dysfunction, microbiome dysbiosis, underlying CRS, and asthma. It also evaluates current therapeutic strategies such as biologics, aspirin therapy after desensitization (ATAD), and endoscopic sinus surgery (ESS). Biologics have shown their effectiveness and safety in the treatment of asthma and CRS. Dupilumab, mepolizumab, depemokimab, and omalizumab have emerged as transformative therapies, particularly for patients with severe type 2 inflammation. Tezepelulumab is effective for both T2-high and T2-low asthma and CRSwNP. Itepekimab has shown its effect in asthma and is under investigation for CRSwNP. Omalizumab is effective in allergic asthma and CRSwNP. ATAD provides an additional disease-modifying approach for N-ERD, though patient adherence and tolerability remain critical challenges. ESS significantly improves asthma control, reduces medication use, and enhances sinonasal outcomes, particularly in severe asthma cases; however, these patients often need recurring surgeries. Despite these advances, treatment outcomes vary based on individual phenotypes and endotypes, underscoring the need for personalized approaches. The report highlights gaps in the literature, such as the lack of head-to-head trials comparing biologics, ATAD, and surgery. Future research should focus on refining treatment algorithms, identifying biomarkers for treatment selection, and assessing long-term outcomes to optimize care for patients with CRS, asthma, and N-ERD.</p>","PeriodicalId":122,"journal":{"name":"Allergy","volume":" ","pages":""},"PeriodicalIF":12.0,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Updated Treatment of Non‐Steroidal Anti‐Inflammatory Drug‐Exacerbated Respiratory Disease: How to Decide on Aspirin Therapy After Desensitization or Biologics? When? How? An EAACI Task Force Report 非甾体抗炎药加重呼吸系统疾病的最新治疗:脱敏后如何选择阿司匹林或生物制剂?什么时候?如何?EAACI工作小组报告
IF 12.4 1区 医学 Q1 ALLERGY Pub Date : 2026-02-05 DOI: 10.1111/all.70243
Gülfem E. Çelik, Joanna S. Makowska, Maria Jose Torres, Cristobalina Mayorga, Tanya M. Laidlaw, Alessandra Vultaggio, Sanna Toppila‐Salmi, Ludger Klimek, Aslı Gelincik, Annick Barbaud, Lene H. Garvey, Ömür Aydın, Thomas Eiwegger, Katharine M. Woessner
Nonsteroidal anti‐inflammatory drug (NSAID)‐exacerbated respiratory disease (NSAID‐ERD) is a heterogeneous condition characterized by chronic eosinophilic airway inflammation in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) and asthma whose symptoms are aggravated after ingestion of aspirin and other NSAIDs. As a unique treatment, aspirin treatment after desensitization (ATAD) has been in use for several years after showing the inhibitory effect on CRS symptoms and nasal polyp growth as well as severe asthma. However, in recent years, biologics have also shown to cause a decrease in polyp size as well as associated outcomes such as quality of life. In this manuscript, considerations on choosing the best treatment of NSAID–ERD are laid out based on current literature.
{"title":"Updated Treatment of Non‐Steroidal Anti‐Inflammatory Drug‐Exacerbated Respiratory Disease: How to Decide on Aspirin Therapy After Desensitization or Biologics? When? How? An EAACI Task Force Report","authors":"Gülfem E. Çelik, Joanna S. Makowska, Maria Jose Torres, Cristobalina Mayorga, Tanya M. Laidlaw, Alessandra Vultaggio, Sanna Toppila‐Salmi, Ludger Klimek, Aslı Gelincik, Annick Barbaud, Lene H. Garvey, Ömür Aydın, Thomas Eiwegger, Katharine M. Woessner","doi":"10.1111/all.70243","DOIUrl":"https://doi.org/10.1111/all.70243","url":null,"abstract":"Nonsteroidal anti‐inflammatory drug (NSAID)‐exacerbated respiratory disease (NSAID‐ERD) is a heterogeneous condition characterized by chronic eosinophilic airway inflammation in patients with chronic rhinosinusitis with nasal polyps (CRSwNP) and asthma whose symptoms are aggravated after ingestion of aspirin and other NSAIDs. As a unique treatment, aspirin treatment after desensitization (ATAD) has been in use for several years after showing the inhibitory effect on CRS symptoms and nasal polyp growth as well as severe asthma. However, in recent years, biologics have also shown to cause a decrease in polyp size as well as associated outcomes such as quality of life. In this manuscript, considerations on choosing the best treatment of NSAID–ERD are laid out based on current literature.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"6 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146122100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CD4 + T Cell‐Intrinsic Arg1 Regulates Th1 Dynamics in Influenza: Functional and Translational Implications for Infection and Cancer Inflammation CD4 + T细胞-内在Arg1调节流感中Th1的动态:感染和癌症炎症的功能和翻译意义
IF 12.4 1区 医学 Q1 ALLERGY Pub Date : 2026-02-05 DOI: 10.1111/all.70249
Anishaa Balaji, Sophia N. Karagiannnis, Alexandra J. McCraw
{"title":"CD4 + T Cell‐Intrinsic Arg1 Regulates Th1 Dynamics in Influenza: Functional and Translational Implications for Infection and Cancer Inflammation","authors":"Anishaa Balaji, Sophia N. Karagiannnis, Alexandra J. McCraw","doi":"10.1111/all.70249","DOIUrl":"https://doi.org/10.1111/all.70249","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"22 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146122101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Microarrayed Allergen Molecules Distinguish IgE Sensitisation to Blomia tropicalis and Dermatophagoides pteronyssinus 微阵列变应原分子区分对热带布洛姆和翼状棘球绦虫的IgE致敏
IF 12.4 1区 医学 Q1 ALLERGY Pub Date : 2026-02-04 DOI: 10.1111/all.70232
Nishelle Dsouza, Siratcha Phanthong, Huey‐Jy Huang, Milena Weber, Eszter Sarzsinszky, Petra Zieglmayer, Gabrielle Pauli, Margarete Focke‐Tejkl, Mikhail Tulaev, Nikolina Todorovic, Walter Keller, Thomas Schlederer, Luis Caraballo, Anchalee Tungtrongchitr, Rudolf Valenta, Pongsakorn Tantilipikorn, Susanne Vrtala
Background House dust mites (HDMs) are the most important respiratory allergen sources. In temperate regions, the genus Dermatophagoides predominates, whereas in sub‐tropical and tropical regions, the genus Blomia is also of high importance. There is only limited IgE cross‐reactivity between Dermatophagoides and Blomia . Objective To produce a chip containing purified microarrayed Blomia tropicalis (Blo t) and Dermatophagoides pteronyssinus allergens (Der p) capable of identifying patients with a genuine Blo t or Der p IgE sensitisation, co‐sensitisation and/or cross‐sensitisation. Methods Chips containing seven purified Blo t and thirteen Der p allergens were generated by microarray technology and tested for IgE and IgG reactivity in HDM ‐sensitised patients from Blo t‐endemic (group 1: n = 115) and Blo t‐non‐endemic (group 2: n = 33) regions. IgE cross‐reactivity was analysed by IgE inhibition studies. Results IgE levels to Blo t 2, Blo t 5, Blo t 10, Blo t 12 and Blo t 21 were significantly higher in HDM‐sensitised patients from Blo t‐endemic as compared to patients from Blo t‐non‐endemic regions, whereas the opposite was observed for IgE to Der p 2 and Der p 21 in patients from Blo t‐non‐endemic regions. An algorithm based on IgE reactivity profiles and allergen‐specific IgE levels capable of discriminating genuine sensitisation to Blo t and Der p or co‐sensitisation was established. In HDM‐sensitised patients from Blo t‐endemic regions, each of the aforementioned sensitisation profiles was observed, whereas in HDM‐sensitised patients from Blo t‐non‐endemic regions, only genuine sensitisations to Der p and co‐sensitisations to Blo t and Der p were observed. Conclusion The algorithm based on microarrayed Blo t and Der p allergens for discrimination of Blo t and Der p sensitisation may support prescription of allergen‐specific immunotherapy. At minimum, it will be helpful in understanding disease aetiology and for fine resolution mapping of allergic reactivities in HDM sensitisation.
室内尘螨是最重要的呼吸道过敏原。在温带地区,Dermatophagoides属占主导地位,而在亚热带和热带地区,Blomia属也很重要。皮肤噬螨和Blomia之间只有有限的IgE交叉反应性。目的制备一种含有纯化的微阵列热带布洛米氏菌(Blo t)和翼状窦皮噬菌(derp)过敏原的芯片,能够识别真正的Blo t或Der p IgE致敏、共致敏和/或交叉致敏患者。方法采用微阵列技术制备含有7个纯化的Blo t和13个Der p过敏原的芯片,检测来自Blo t流行区(组1:n = 115)和非Blo t流行区(组2:n = 33)的HDM敏感患者的IgE和IgG反应性。通过IgE抑制研究分析IgE交叉反应性。结果与Blo - t非流行地区的患者相比,来自Blo - t流行地区的HDM敏感患者的Blo - t 2、Blo - t 5、Blo - t 10、Blo - t 12和Blo - t 21的IgE水平显著高于来自Blo - t非流行地区的患者,而来自Blo - t非流行地区的患者的IgE水平与之相反。建立了一种基于IgE反应性谱和过敏原特异性IgE水平的算法,该算法能够区分blot和Der p的真正致敏或共致敏。在来自blot流行地区的HDM致敏患者中,观察到上述每种致敏特征,而在来自blot非流行地区的HDM致敏患者中,仅观察到对Der p的真实致敏以及对blot和Der p的共致敏。结论基于微阵列blot和Der p过敏原的blot和Der p致敏区分算法可为过敏原特异性免疫治疗处方提供支持。至少,这将有助于了解疾病的病因,并为HDM致敏的过敏反应绘制精细分辨率图。
{"title":"Microarrayed Allergen Molecules Distinguish IgE Sensitisation to Blomia tropicalis and Dermatophagoides pteronyssinus","authors":"Nishelle Dsouza, Siratcha Phanthong, Huey‐Jy Huang, Milena Weber, Eszter Sarzsinszky, Petra Zieglmayer, Gabrielle Pauli, Margarete Focke‐Tejkl, Mikhail Tulaev, Nikolina Todorovic, Walter Keller, Thomas Schlederer, Luis Caraballo, Anchalee Tungtrongchitr, Rudolf Valenta, Pongsakorn Tantilipikorn, Susanne Vrtala","doi":"10.1111/all.70232","DOIUrl":"https://doi.org/10.1111/all.70232","url":null,"abstract":"Background House dust mites (HDMs) are the most important respiratory allergen sources. In temperate regions, the genus <jats:italic>Dermatophagoides</jats:italic> predominates, whereas in sub‐tropical and tropical regions, the genus <jats:italic>Blomia</jats:italic> is also of high importance. There is only limited IgE cross‐reactivity between <jats:italic>Dermatophagoides</jats:italic> and <jats:italic>Blomia</jats:italic> . Objective To produce a chip containing purified microarrayed <jats:italic>Blomia tropicalis</jats:italic> (Blo t) and <jats:italic>Dermatophagoides pteronyssinus</jats:italic> allergens (Der p) capable of identifying patients with a genuine Blo t or Der p <jats:styled-content style=\"fixed-case\">IgE</jats:styled-content> sensitisation, co‐sensitisation and/or cross‐sensitisation. Methods Chips containing seven purified Blo t and thirteen Der p allergens were generated by microarray technology and tested for <jats:styled-content style=\"fixed-case\">IgE</jats:styled-content> and <jats:styled-content style=\"fixed-case\">IgG</jats:styled-content> reactivity in <jats:styled-content style=\"fixed-case\">HDM</jats:styled-content> ‐sensitised patients from Blo t‐endemic (group 1: <jats:italic>n</jats:italic> = 115) and Blo t‐non‐endemic (group 2: <jats:italic>n</jats:italic> = 33) regions. <jats:styled-content style=\"fixed-case\">IgE</jats:styled-content> cross‐reactivity was analysed by <jats:styled-content style=\"fixed-case\">IgE</jats:styled-content> inhibition studies. Results IgE levels to Blo t 2, Blo t 5, Blo t 10, Blo t 12 and Blo t 21 were significantly higher in HDM‐sensitised patients from Blo t‐endemic as compared to patients from Blo t‐non‐endemic regions, whereas the opposite was observed for IgE to Der p 2 and Der p 21 in patients from Blo t‐non‐endemic regions. An algorithm based on IgE reactivity profiles and allergen‐specific IgE levels capable of discriminating genuine sensitisation to Blo t and Der p or co‐sensitisation was established. In HDM‐sensitised patients from Blo t‐endemic regions, each of the aforementioned sensitisation profiles was observed, whereas in HDM‐sensitised patients from Blo t‐non‐endemic regions, only genuine sensitisations to Der p and co‐sensitisations to Blo t and Der p were observed. Conclusion The algorithm based on microarrayed Blo t and Der p allergens for discrimination of Blo t and Der p sensitisation may support prescription of allergen‐specific immunotherapy. At minimum, it will be helpful in understanding disease aetiology and for fine resolution mapping of allergic reactivities in HDM sensitisation.","PeriodicalId":122,"journal":{"name":"Allergy","volume":"8 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146115728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Algorithms in Allergy: Hereditary Angioedema 过敏的算法:遗传性血管性水肿
IF 12.4 1区 医学 Q1 ALLERGY Pub Date : 2026-02-03 DOI: 10.1111/all.70241
Konrad Bork, Markus Magerl, Emel Aygören‐Pürsün, Henriette Farkas
{"title":"Algorithms in Allergy: Hereditary Angioedema","authors":"Konrad Bork, Markus Magerl, Emel Aygören‐Pürsün, Henriette Farkas","doi":"10.1111/all.70241","DOIUrl":"https://doi.org/10.1111/all.70241","url":null,"abstract":"","PeriodicalId":122,"journal":{"name":"Allergy","volume":"16 1","pages":""},"PeriodicalIF":12.4,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146101361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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