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A partial loss-of-function variant in STAT6 protects against T2 asthma. STAT6的部分功能缺失变体可预防T2哮喘。
IF 14.2 1区 医学 Q1 ALLERGY Pub Date : 2024-10-16 DOI: 10.1016/j.jaci.2024.10.002
Katla Kristjansdottir,Guðmundur L Norddahl,Erna V Ivarsdottir,Gisli H Halldorsson,Gudmundur Einarsson,Kristbjörg Bjarnadóttir,Gudrun Rutsdottir,Asgeir O Arnthorsson,Christian Erikstrup,Steinunn Gudmundsdottir,Kristbjorg Gunnarsdottir,María I Gunnbjornsdottir,Bjarni V Halldorsson,Hilma Holm,Dora Ludviksdottir,Bjorn R Ludviksson,Søren Brunak,Mie Topholm Bruun,Christina Mikkelsen,Susan Mikkelsen,Bitten Aagaard Jensen,Erik Sørensen,Simon Francis Thomsen,Henrik Ullum,Isleifur Olafsson,Pall T Onundarson,Sisse Rye Ostrowski,Saedis Saevarsdottir,Olof Sigurdardottir,Bardur Sigurgeirsson,Audunn S Snaebjarnarson,Gardar Sveinbjornsson,Gudny E Thorlacius,Gudmar Thorleifsson,Vinicius Tragante,Brynjar Vidarsson,Celeste Porsbjerg,Unnur S Bjornsdottir,Patrick Sulem,Daniel F Gudbjartsson,Pall Melsted,Ole Bv Pedersen,Ingileif Jonsdóttir,Thorunn A Olafsdottir,Kari Stefansson
BACKGROUNDSignal Transducer and Activator of Transcription 6 (STAT6) is central to Type 2 (T2) inflammation and common non-coding variants at the STAT6 locus associate with various T2 inflammatory traits, including diseases, and its pathway is widely targeted in asthma treatment.OBJECTIVETo test the association of a rare missense variant in STAT6, p.L406P, with T2 inflammatory traits, including the risk of asthma and allergic diseases, and to characterize its functional consequences in cell culture.METHODSWe tested association of p.L406P with plasma protein levels, white blood cell counts and the risk of asthma and allergic phenotypes. We tested significant associations in other cohorts using a burden test. The effects of p.L406P on STAT6 protein function were examined in cell lines and by comparing CD4+ T-cell responses from carriers and non-carriers of the variant.RESULTSp.L406P associated with reduced plasma levels of STAT6 and IgE as well as with lower eosinophil and basophil counts in blood. It also protected against asthma, mostly driven by severe T2 high asthma. We showed that p.L406P led to lower IL-4-induced activation in luciferase reporter assays and lower levels of STAT6 in CD4+ T cells. We identified multiple genes with expression that was affected by the p.L406P genotype upon IL-4 treatment of CD4+ T cells; the effect was consistent with a weaker IL-4 response in carriers than non-carriers of p.L406P.CONCLUSIONSWe report a partial loss-of-function variant in STAT6, resulting in dampened IL-4 responses and protection from T2 high asthma, implicating STAT6 as an attractive therapeutic target.
背景信号转导和转录激活因子 6(STAT6)是 2 型(T2)炎症的核心,STAT6 基因座上常见的非编码变异与包括疾病在内的各种 T2 炎症特征相关,其通路被广泛地作为哮喘治疗的靶点。我们检测了 p.L406P 与血浆蛋白水平、白细胞计数以及哮喘和过敏表型风险的关系。我们使用负荷试验检测了其他队列中的重大关联。结果p.L406P 与血浆中 STAT6 和 IgE 水平降低以及血液中嗜酸性粒细胞和嗜碱性粒细胞计数降低有关。它还能预防哮喘,主要是严重的 T2 高哮喘。我们发现,p.L406P 会降低荧光素酶报告实验中 IL-4 诱导的激活,并降低 CD4+ T 细胞中 STAT6 的水平。我们发现了多个基因,这些基因的表达在 CD4+ T 细胞接受 IL-4 处理时会受到 p.L406P 基因型的影响;这种影响与 p.L406P 基因携带者的 IL-4 反应弱于非携带者是一致的。
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引用次数: 0
Role of DOCK8 in Cytokine Storm Syndromes. DOCK8 在细胞因子风暴综合征中的作用
IF 14.2 1区 医学 Q1 ALLERGY Pub Date : 2024-10-16 DOI: 10.1016/j.jaci.2024.10.004
Mingce Zhang,Remy R Cron,Niansheng Chu,Junior Nguyen,Scott M Gordon,Esraa M Eloseily,T Prescott Atkinson,Peter Weiser,Mark R Walter,Portia A Kreiger,Scott W Canna,Edward M Behrens,Randy Q Cron
BACKGROUNDCytokine storm syndromes (CSS), including hemophagocytic lymphohistiocytosis (HLH), are increasingly recognized as hyperinflammatory states leading to multi-organ failure and death. Familial HLH (FHL) in infancy results from homozygous genetic defects in perforin-mediated cytolysis by CD8 T-lymphocytes and natural killer (NK) cells. Later onset CSS are frequently associated with heterozygous defects in FHL genes, but genetic etiologies for most are unknown. We identified rare DOCK8 variants in CSS patients.OBJECTIVEWe explore the role of CSS patient-derived DOCK8 mutations on cytolytic activity in NK cells. We further study effects of DOCK8 deficiency in murine models of CSS.METHODSDOCK8 cDNA from 2 unrelated CSS patients with different missense mutations were introduced into human NK-92 NK cells by foamy virus transduction. NK cell degranulation (CD107a), cytolytic activity against K562 target cells, and interferon-gamma (IFNγ) production were explored by flow cytometry. A third CSS patient DOCK8 mRNA splice acceptor site variant was explored by exon trapping. Dock8-/- mice were assessed for features of CSS (weight loss, splenomegaly, hepatic inflammation, cytopenias, and IFNγ levels) upon challenge with lymphocytic choriomeningitis virus (LCMV) and excess IL-18.RESULTSBoth patient DOCK8 missense mutations decreased cytolytic function in NK cells in a partial dominant-negative fashion in vitro. The patient DOCK8 splice variant disrupted mRNA splicing in vitro. LCMV infection promoted CSS in Dock8-/- mice and interacted with excess IL-18 limiting T-cell numbers while promoting CD8 T-cell hyperactivation.CONCLUSIONMutations in DOCK8 may contribute to CSS-like hyperinflammatory states by altering cytolytic function in a threshold model of disease.
背景细胞因子风暴综合征(Cytokine storm syndromes,CSS),包括嗜血细胞淋巴组织细胞增生症(hemophagocytic lymphohistiocytosis,HLH),越来越多地被认为是导致多器官衰竭和死亡的高炎症状态。婴儿期的家族性 HLH(FHL)是由于 CD8 T 淋巴细胞和自然杀伤(NK)细胞介导的穿孔素细胞溶解的同基因缺陷造成的。晚发 CSS 常与 FHL 基因的杂合性缺陷有关,但大多数的遗传病因不明。我们在 CSS 患者中发现了罕见的 DOCK8 变异。目的 我们探讨了 CSS 患者来源的 DOCK8 变异对 NK 细胞溶解活性的作用。我们进一步研究了DOCK8缺乏对小鼠CSS模型的影响。方法通过泡沫病毒转导,将来自2名无关CSS患者、具有不同错义突变的DOCK8 cDNA导入人NK-92 NK细胞。通过流式细胞术检测了 NK 细胞脱颗粒(CD107a)、对 K562 靶细胞的细胞溶解活性以及γ干扰素(IFNγ)的产生。通过外显子诱捕法研究了第三种 CSS 患者 DOCK8 mRNA 剪接受体位点变异。在淋巴细胞性脉络膜炎病毒(LCMV)和过量 IL-18 的挑战下,评估了 Dock8-/- 小鼠的 CSS 特征(体重减轻、脾脏肿大、肝脏炎症、细胞减少和 IFNγ 水平)。患者的 DOCK8 剪接变体在体外破坏了 mRNA 剪接。LCMV感染促进了Dock8-/-小鼠的CSS,并与过量的IL-18相互作用,限制了T细胞的数量,同时促进了CD8 T细胞的过度激活。
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引用次数: 0
Omics in allergy and asthma. 过敏和哮喘中的分子生物学。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-09 DOI: 10.1016/j.jaci.2024.09.023
Hirohisa Saito, Masato Tamari, Kenichiro Motomura, Masashi Ikutani, Susumu Nakae, Kenji Matsumoto, Hideaki Morita

This review explores the transformative impact of omics technologies on allergy and asthma research in recent years, focusing on advancements in high-throughput technologies related to genomics and transcriptomics. In particular, the rapid spread of single-cell RNA sequencing has markedly advanced our understanding of the molecular pathology of allergic diseases. Furthermore, high-throughput genome sequencing has accelerated the discovery of monogenic disorders that were previously overlooked as ordinary intractable allergic diseases. We also introduce microbiomics, proteomics, lipidomics, and metabolomics, which are quickly growing areas of research interest, although many of their current findings remain inconclusive as solid evidence. By integrating these omics data, we will gain deeper insights into disease mechanisms, leading to the development of precision medicine approaches that promise to enhance treatment outcomes.

本综述探讨了近年来omics技术对过敏和哮喘研究的变革性影响,重点关注与基因组学和转录组学相关的高通量技术的进展。尤其是单细胞 RNA 测序技术的迅速普及极大地促进了我们对过敏性疾病分子病理学的了解。此外,高通量基因组测序加速了单基因疾病的发现,而这些疾病以前被忽视为普通的难治性过敏性疾病。我们还介绍了微生物组学、蛋白质组学、脂质组学和代谢组学,这些领域的研究兴趣正在迅速增长,尽管它们目前的许多研究结果还不能作为确凿的证据。通过整合这些 omics 数据,我们将对疾病机制有更深入的了解,从而开发出有望提高治疗效果的精准医疗方法。
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引用次数: 0
IL-4 and dendritic cells in atopic dermatitis: Old dogs learn new tricks. 特应性皮炎中的 IL-4 和树突状细胞:老狗学新招
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-09 DOI: 10.1016/j.jaci.2024.10.001
Donata Vercelli
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引用次数: 0
The rs6967330 minor allele in CDHR3 is a significant risk factor for severe acute exacerbations in chronic rhinosinusitis. CDHR3 的小等位基因 rs6967330 是 CRS 严重急性加重的重要风险因素。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-09 DOI: 10.1016/j.jaci.2024.09.025
Sunny Palumbo, Joseph Irish, Nirushan Narendran, Debra A Stern, Sophia Volpe, Christopher H Le, Rebekah Starks, Anthony Bosco, Fernando D Martinez, Eugene H Chang

Background: Acute exacerbations of chronic rhinosinusitis (AECRS) are commonly triggered by rhinovirus (RV) infections with secondary bacterial infections. Risk factors for AECRS are not well understood.

Objective: We sought to determine whether carriers of the minor allele rs6967330 (AA/AG) in the cadherin-related family member 3 (CDHR3) gene have an increased risk for RV infections in AECRS in vivo and identify CDHR3 genotype-dependent host responses to RV infection in differentiated nasal airway-liquid interface (ALI) cultures ex vivo.

Methods: We performed a prospective year-long study of adult subjects with chronic rhinosinusitis by the rs6967330 genotype (AA/AG, n = 16; GG, n = 38). We contacted subjects every 2 weeks, and if they reported AECRS, then clinical data were collected. ALI cultures of adults with chronic rhinosinusitis (AG/AA, n = 19; GG, n = 19) were challenged with RV-A and RV-C. We measured viral copy numbers at 4 and 48 hours postinfection and RNA transcriptomes and cytokines at 48 hours postinfection.

Results: Subjects with the minor allele had significantly higher rates of RV and bacterial infections than those with the major allele. ALI minor allele cultures had higher viral copy numbers of RV-A and RV-C after 48 hours compared with the major allele. Differentially expressed genes and pathways identified an upregulation of IL-10 and IL-4/IL-13 pathways and a significant downregulation of Toll-like receptor pathways in the minor allele cultures after RV-A and RV-C infection. Unsupervised hierarchical analysis of all differentially expressed genes suggested that allergic rhinitis had an additive effect on this response.

Conclusions: The rs6967330 minor allele is associated with increased RV-A and RV-C replication, downregulation of Toll-like receptor-mediated responses, and increased type-2 and cytokine and chemokine responses during RV infection.

背景:慢性鼻炎急性加重期(AECRS)通常由鼻病毒(RV)感染和继发细菌感染引发。AECRS的风险因素尚不十分清楚:目的:确定Cadherin相关家族成员3(CDHR3)基因的小等位基因rs6967330(AA/AG)携带者是否会增加体内AECRS感染RV的风险,并在体内分化的鼻腔气道液体界面(ALI)培养物中确定CDHR3基因型依赖的宿主对RV感染的反应:我们对患有慢性鼻炎(CRS)的成年受试者进行了一项为期一年的前瞻性研究,研究对象的基因型为 rs6967330(AA/AG,n=16;GG,n=38)。我们每两周与受试者联系一次,如果他们报告了 AECRS,则收集他们的临床数据。用 RV-A 和 RV-C 对患有 CRS 的成人(AG/AA,n=19;GG,n=19)进行 ALI 培养。我们测量了感染后 4 小时和 48 小时的病毒拷贝数以及感染后 48 小时的 RNA 转录组和细胞因子:结果:小等位基因受试者的 RV 和细菌感染率明显高于大等位基因受试者。48小时后,ALI小等位基因培养物的RV-A和RV-C病毒拷贝数高于大等位基因培养物。在RV-A和RV-C感染后,小等位基因培养物中的差异表达基因(DEG)和通路确定了IL-10和IL4/13通路的上调以及类似收费受体(TLR)通路的显著下调。对所有 DEGs 的无监督分层分析表明,过敏性鼻炎对这种反应有叠加效应:rs6967330小等位基因与RV-A和RV-C复制增加、TLR介导的反应下调以及RV感染期间T2型、细胞因子和趋化因子反应增加有关。
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引用次数: 0
Differential Tfh cell phenotypes distinguish IgE-mediated milk allergy from eosinophilic esophagitis in children. 不同的 Tfh 细胞表型可区分 IgE 介导的牛奶过敏和儿童嗜酸性粒细胞食管炎。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-08 DOI: 10.1016/j.jaci.2024.09.024
Daniel Lozano-Ojalvo, Xin Chen, Wajiha Kazmi, David Menchén-Martínez, Leticia Pérez-Rodríguez, Weslley Fernandes-Braga, Scott Tyler, Keith Benkov, Nanci Pittman, Joanne Lai, Hugh A Sampson, Maria Curotto de Lafaille, David Dunkin, M Cecilia Berin

Background: IgE-mediated food allergy and eosinophilic esophagitis (EoE) are diseases commonly triggered by milk. Milk-responsive CD4+ T cells producing type 2 cytokines are present in both diseases, yet the clinical manifestation of disease in milk allergy (MA) and EoE are distinct.

Objective: To identify CD4+ T cell differences between EoE and MA that may be responsible for distinct disease manifestations.

Methods: The total and milk-specific CD4+ T cell phenotype of children with milk allergy (MA), EoE (active or in remission) and controls was measured using spectral flow cytometry of peripheral blood (all groups) or esophageal biopsies (EoE and control).

Results: Circulating milk-responsive T cells could be identified in active (A)-EoE and MA. An increased frequency of Th2A cells was also noted in MA and EoE. In circulating T cells, type 2 cytokine production was elevated in MA, but not EoE. Within the milk-responsive Tfh subset, a dichotomy of phenotype was noted: Tfh13 cells predominated in MA, while IL-10-producing Tfh cells predominated in EoE. In the esophagus, CD4+ T cells were constitutively activated and expressed not only type 2 cytokines, but also IL-10 and IL-21 in A-EoE. There was production of IgG4 from CD38+ plasma cells in close proximity to CD4+ T cells. In vitro activation studies demonstrated that IL-10 and IL-21 elicited strong IgG4 responses in B lymphocytes, while IL-4 and IL-13 promoted IgE production.

Conclusion: Our studies demonstrate a dichotomy of Tfh responses that may be the basis for the different clinical manifestations to milk in EoE and MA.

背景:IgE介导的食物过敏和嗜酸性粒细胞食管炎(EoE)是由牛奶引发的常见疾病。这两种疾病中都存在产生 2 型细胞因子的牛奶反应性 CD4+ T 细胞,但牛奶过敏(MA)和嗜酸性粒细胞性食管炎的临床表现却截然不同:目的:确定牛奶过敏和肠易激综合征的 CD4+ T 细胞差异可能是导致不同疾病表现的原因:方法:使用光谱流式细胞术测量外周血(所有组别)或食管活检组织(EoE 和对照组)中牛奶过敏(MA)、EoE(活动期或缓解期)和对照组儿童的总 CD4+ T 细胞表型和牛奶特异性 CD4+ T 细胞表型:结果:在活动性(A)-EoE 和 MA 中可发现循环牛奶反应性 T 细胞。在 MA 和 EoE 中,Th2A 细胞的频率也有所增加。在循环 T 细胞中,2 型细胞因子的产生在 MA 中升高,但在 EoE 中没有升高。在牛奶反应性 Tfh 亚群中,发现了表型的二分法:在 MA 中以 Tfh13 细胞为主,而在 EoE 中则以产生 IL-10 的 Tfh 细胞为主。在食管中,CD4+ T 细胞被持续激活,不仅表达 2 型细胞因子,而且在急性食管炎中还表达 IL-10 和 IL-21。CD38+ 浆细胞在靠近 CD4+ T 细胞处产生 IgG4。体外活化研究表明,IL-10 和 IL-21 在 B 淋巴细胞中引起强烈的 IgG4 反应,而 IL-4 和 IL-13 则促进 IgE 的产生:我们的研究证明了Tfh反应的二分法,这可能是EoE和MA患者对牛奶的不同临床表现的基础。
{"title":"Differential Tfh cell phenotypes distinguish IgE-mediated milk allergy from eosinophilic esophagitis in children.","authors":"Daniel Lozano-Ojalvo, Xin Chen, Wajiha Kazmi, David Menchén-Martínez, Leticia Pérez-Rodríguez, Weslley Fernandes-Braga, Scott Tyler, Keith Benkov, Nanci Pittman, Joanne Lai, Hugh A Sampson, Maria Curotto de Lafaille, David Dunkin, M Cecilia Berin","doi":"10.1016/j.jaci.2024.09.024","DOIUrl":"https://doi.org/10.1016/j.jaci.2024.09.024","url":null,"abstract":"<p><strong>Background: </strong>IgE-mediated food allergy and eosinophilic esophagitis (EoE) are diseases commonly triggered by milk. Milk-responsive CD4<sup>+</sup> T cells producing type 2 cytokines are present in both diseases, yet the clinical manifestation of disease in milk allergy (MA) and EoE are distinct.</p><p><strong>Objective: </strong>To identify CD4<sup>+</sup> T cell differences between EoE and MA that may be responsible for distinct disease manifestations.</p><p><strong>Methods: </strong>The total and milk-specific CD4<sup>+</sup> T cell phenotype of children with milk allergy (MA), EoE (active or in remission) and controls was measured using spectral flow cytometry of peripheral blood (all groups) or esophageal biopsies (EoE and control).</p><p><strong>Results: </strong>Circulating milk-responsive T cells could be identified in active (A)-EoE and MA. An increased frequency of Th2A cells was also noted in MA and EoE. In circulating T cells, type 2 cytokine production was elevated in MA, but not EoE. Within the milk-responsive Tfh subset, a dichotomy of phenotype was noted: Tfh13 cells predominated in MA, while IL-10-producing Tfh cells predominated in EoE. In the esophagus, CD4<sup>+</sup> T cells were constitutively activated and expressed not only type 2 cytokines, but also IL-10 and IL-21 in A-EoE. There was production of IgG4 from CD38<sup>+</sup> plasma cells in close proximity to CD4<sup>+</sup> T cells. In vitro activation studies demonstrated that IL-10 and IL-21 elicited strong IgG4 responses in B lymphocytes, while IL-4 and IL-13 promoted IgE production.</p><p><strong>Conclusion: </strong>Our studies demonstrate a dichotomy of Tfh responses that may be the basis for the different clinical manifestations to milk in EoE and MA.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":null,"pages":null},"PeriodicalIF":11.4,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400312","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
JAK-STAT signaling pathway, immunodeficiency, inflammation, immune dysregulation, and inborn errors of immunity. 干扰人类 JAK-STAT 信号的先天性免疫错误和体细胞变异表型。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-04 DOI: 10.1016/j.jaci.2024.09.020
Simran Samra, Jenna R E Bergerson, Alexandra F Freeman, Stuart E Turvey

The Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling cascade is an evolutionarily conserved signal transduction pathway that regulates many vital cellular processes, including immune function and hematopoiesis. Human genetic variants that disrupt JAK-STAT signaling are being found to cause a rapidly increasing number of diseases, including both germline-encoded inborn errors of immunity (IEI) and acquired somatic variants, causing a so-called phenocopy of the IEI. Multiple genetic mechanisms are responsible for this growing group of JAK-STAT diseases including loss-of-function, gain-of-function, and dominant negative effects. In this review, we discuss the clinical presentation and pathogenesis of all currently described JAK-STAT defects, as well as provide an overview of the guiding principles to consider in diagnosing and treating these conditions.

Janus 激酶-信号转导和转录激活因子(JAK-STAT)信号级联是一种进化保守的信号转导途径,它调节着许多重要的细胞过程,包括免疫功能和造血功能。目前发现,干扰 JAK-STAT 信号转导的人类基因变异会导致越来越多的疾病,包括基因编码的先天性免疫错误(IEI)和导致 IEI "表型复制 "的获得性体细胞变异。多种遗传机制导致了越来越多的 JAK-STAT 疾病,包括功能缺失(LOF)、功能获得(GOF)和显性负(DN)效应。在这篇综述中,我们将讨论目前描述的所有 JAK/STAT 缺陷的临床表现和发病机制,并概述诊断和治疗这些疾病时应考虑的指导原则。
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引用次数: 0
Opportunities for using artificial intelligence in air pollution and health research. 在空气污染与健康研究中使用人工智能的机遇。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-03 DOI: 10.1016/j.jaci.2024.09.022
Roger D Peng, Sarah E Chambliss
{"title":"Opportunities for using artificial intelligence in air pollution and health research.","authors":"Roger D Peng, Sarah E Chambliss","doi":"10.1016/j.jaci.2024.09.022","DOIUrl":"10.1016/j.jaci.2024.09.022","url":null,"abstract":"","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":null,"pages":null},"PeriodicalIF":11.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142377929","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
Clinical Effectiveness and Safety of Dupilumab in Chronic Obstructive Pulmonary Disease Patients: A 7-Year Population-based Cohort Study. 慢性阻塞性肺病患者使用杜匹单抗的临床有效性和安全性:一项为期 7 年的人群队列研究。
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-03 DOI: 10.1016/j.jaci.2024.09.019
Chuan-Yen Sun, Yohannes Tesfaigzi, Gin-Yi Lee, Yi-Hsuan Chen, Scott T Weiss, Kevin Sheng-Kai Ma

Background: Previous randomized controlled trials had established the efficacy of dupilumab among patients with chronic obstructive pulmonary disease (COPD) treated with triple therapy over 52 weeks of follow-up.

Objective: This population-based cohort study aimed to explore the long-term clinical effectiveness of dupilumab in COPD patients.

Methods: This population-based cohort study included U.S. patients with COPD between April 2017 and August 2024. Patients initiating dupilumab and therapies that incorporated long-acting β2-agonists (LABA) inhalers were included. Patients with asthma or lung cancer were excluded. The risk of outcomes after the initiation of dupilumab versus LABA-containing therapies was measured. For detailed Methods, please see the Methods section in this article's Online Repository at www.jacionline.org.

Results: A total of 1,521 dupilumab initiators and 1,521 propensity score-matched patients receiving LABA-based therapies were included. Dupilumab recipients were associated with lower all-cause mortality (HR:0.53, 95% CI:0.43-0.65), emergency visits (HR:0.78, 95% CI:0.69-0.89), and acute exacerbation (AE) rates (HR:0.59, 95% CI:0.53-0.65). Dupilumab was also associated with reductions in the requirement of short-acting β2-agonists (HR:0.48, 95% CI:0.43-0.52), short-acting muscarinic antagonists (HR:0.43, 95% CI:0.37-0.49) for symptoms control. Additionally, dupilumab decreased subsequent pneumonia (HR:0.65, 95% CI:0.50-0.86), and COPD-relevant comorbidities including new-onset heart failure (HR:0.69, 95% CI:0.53-0.90) and new-onset anxiety (HR:0.70, 95% CI:0.53-0.93).

Conclusions: Dupilumab was associated with a lower rate of mortality, emergency visits, reduced risk of AEs, respiratory symptoms, and respiratory infections in COPD patients. More studies are required to validate the effectiveness of dupilumab among patients with COPD across various severities.

背景:先前的随机对照试验证实了杜匹单抗对接受三联疗法治疗的慢性阻塞性肺病(COPD)患者的疗效:先前的随机对照试验证实,在接受三联疗法治疗的慢性阻塞性肺病(COPD)患者中,杜比单抗在52周的随访期间具有疗效:这项基于人群的队列研究旨在探讨杜比单抗对慢性阻塞性肺病患者的长期临床疗效:这项基于人群的队列研究纳入了2017年4月至2024年8月期间的美国COPD患者。研究纳入了开始使用杜必鲁单抗和长效β2-激动剂(LABA)吸入剂疗法的患者。哮喘或肺癌患者除外。对开始使用杜比单抗与含LABA疗法后的结果风险进行了测量。详细方法请参见本文在线资料库中的方法部分,网址:www.jacionline.org.Results:研究共纳入了1,521名开始使用杜匹鲁单抗的患者和1,521名接受LABA疗法的倾向评分匹配患者。接受杜匹单抗治疗的患者全因死亡率(HR:0.53,95% CI:0.43-0.65)、急诊就诊率(HR:0.78,95% CI:0.69-0.89)和急性加重(AE)率(HR:0.59,95% CI:0.53-0.65)均较低。杜匹鲁单抗还能减少控制症状所需的短效β2-激动剂(HR:0.48,95% CI:0.43-0.52)和短效毒蕈碱拮抗剂(HR:0.43,95% CI:0.37-0.49)。此外,杜匹鲁单抗还可减少继发肺炎(HR:0.65,95% CI:0.50-0.86)和慢性阻塞性肺疾病相关合并症,包括新发心衰(HR:0.69,95% CI:0.53-0.90)和新发焦虑(HR:0.70,95% CI:0.53-0.93):结论:杜匹单抗可降低慢性阻塞性肺病患者的死亡率、急诊就诊率,降低AEs、呼吸道症状和呼吸道感染的风险。还需要更多的研究来验证杜匹单抗对不同严重程度的慢性阻塞性肺病患者的疗效。
{"title":"Clinical Effectiveness and Safety of Dupilumab in Chronic Obstructive Pulmonary Disease Patients: A 7-Year Population-based Cohort Study.","authors":"Chuan-Yen Sun, Yohannes Tesfaigzi, Gin-Yi Lee, Yi-Hsuan Chen, Scott T Weiss, Kevin Sheng-Kai Ma","doi":"10.1016/j.jaci.2024.09.019","DOIUrl":"10.1016/j.jaci.2024.09.019","url":null,"abstract":"<p><strong>Background: </strong>Previous randomized controlled trials had established the efficacy of dupilumab among patients with chronic obstructive pulmonary disease (COPD) treated with triple therapy over 52 weeks of follow-up.</p><p><strong>Objective: </strong>This population-based cohort study aimed to explore the long-term clinical effectiveness of dupilumab in COPD patients.</p><p><strong>Methods: </strong>This population-based cohort study included U.S. patients with COPD between April 2017 and August 2024. Patients initiating dupilumab and therapies that incorporated long-acting β2-agonists (LABA) inhalers were included. Patients with asthma or lung cancer were excluded. The risk of outcomes after the initiation of dupilumab versus LABA-containing therapies was measured. For detailed Methods, please see the Methods section in this article's Online Repository at www.jacionline.org.</p><p><strong>Results: </strong>A total of 1,521 dupilumab initiators and 1,521 propensity score-matched patients receiving LABA-based therapies were included. Dupilumab recipients were associated with lower all-cause mortality (HR:0.53, 95% CI:0.43-0.65), emergency visits (HR:0.78, 95% CI:0.69-0.89), and acute exacerbation (AE) rates (HR:0.59, 95% CI:0.53-0.65). Dupilumab was also associated with reductions in the requirement of short-acting β2-agonists (HR:0.48, 95% CI:0.43-0.52), short-acting muscarinic antagonists (HR:0.43, 95% CI:0.37-0.49) for symptoms control. Additionally, dupilumab decreased subsequent pneumonia (HR:0.65, 95% CI:0.50-0.86), and COPD-relevant comorbidities including new-onset heart failure (HR:0.69, 95% CI:0.53-0.90) and new-onset anxiety (HR:0.70, 95% CI:0.53-0.93).</p><p><strong>Conclusions: </strong>Dupilumab was associated with a lower rate of mortality, emergency visits, reduced risk of AEs, respiratory symptoms, and respiratory infections in COPD patients. More studies are required to validate the effectiveness of dupilumab among patients with COPD across various severities.</p>","PeriodicalId":14936,"journal":{"name":"Journal of Allergy and Clinical Immunology","volume":null,"pages":null},"PeriodicalIF":11.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142377928","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
Role of anti-IgE in immediate drug allergy. 抗 IgE 在药物过敏中的作用
IF 11.4 1区 医学 Q1 ALLERGY Pub Date : 2024-10-02 DOI: 10.1016/j.jaci.2024.09.021
Lily Li, Kimberly G Blumenthal
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引用次数: 0
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Journal of Allergy and Clinical Immunology
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