Journal of Leukocyte Biology最新文献_第2页

Mapping the sepsis immune landscape across age and source of infection: lessons from single-cell multi-omics. 绘制脓毒症免疫景观跨越年龄和感染来源：从单细胞多组学的教训。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag037

Mihir R Atreya, Basilia Zingarelli

引用次数: 0

Neutrophil FcγRI expression as a determinant of oxidative responses in human blood. 中性粒细胞fc γ - ri表达在人血液中氧化反应的决定因素。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag048

Sandrine Huot, Paul R Fortin, Cynthia Laflamme, Marc Pouliot

{"title":"Neutrophil FcγRI expression as a determinant of oxidative responses in human blood.","authors":"Sandrine Huot, Paul R Fortin, Cynthia Laflamme, Marc Pouliot","doi":"10.1093/jleuko/qiag048","DOIUrl":"10.1093/jleuko/qiag048","url":null,"abstract":"Neutrophils express Fc receptors on their surface to trap immune complexes. While the roles of FcγRIIa and FcγRIIIb have been extensively studied in that context, that of FcγRI remains elusive. Recently, aggregated IgGs have been shown to induce rapid FcγRI up-regulation and reactive oxygen species (ROS) generation, but the biological relevance of this process is still unclear. In this study, incubation of blood samples from healthy volunteers with heat-aggregated IgGs, used as a model of immune complexes, rapidly up-regulated the surface expression of FcγRI, predominantly on neutrophils, as measured by flow cytometry. Stimulation of isolated neutrophils with aggregated IgGs resulted in the production of ROS in an FcγRI-dependent fashion, as monitored with a luminol-based chemiluminescence assay. Cytochalasin B potentiated FcγRI expression and ROS production. In resting blood, positive correlations between neutrophil FcγRI and ROS production were observed, both in healthy volunteers and patients with lupus. This study unveils a potentially central regulatory role for neutrophil FcγRI in ROS production, both in healthy individuals and patients with lupus, and identifies neutrophil FcγRI as a promising target to modulate oxidative response.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

CCDC137 stabilizes S100A6 to activate the PI3K/AKT pathway and drive acute myeloid leukemia progression. CCDC137稳定S100A6，激活PI3K/AKT通路，推动急性髓系白血病进展。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag040

Xiaoying Zhao, Wenjing Zhang, Sirui Chen, Xu Dai, Xiang Yu, Mengzhuo Zheng, Yan Wang, Yajing Ma, Jiang Cheng, Weiwei Zheng

引用次数: 0

Transforming growth factor Beta/Smad3/GATA3 axis mediates the therapeutic effect of Ephedra sinica Stapf polysaccharide in allergic rhinitis. 转化生长因子β /Smad3/GATA3轴介导麻黄多糖对变应性鼻炎的治疗作用

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag023

Jingfei Zhang, Zhixuan Wu, Ru Zhang

{"title":"Transforming growth factor Beta/Smad3/GATA3 axis mediates the therapeutic effect of Ephedra sinica Stapf polysaccharide in allergic rhinitis.","authors":"Jingfei Zhang, Zhixuan Wu, Ru Zhang","doi":"10.1093/jleuko/qiag023","DOIUrl":"10.1093/jleuko/qiag023","url":null,"abstract":"Allergic rhinitis (AR) is a prevalent inflammatory disorder with limited therapeutic options. Ephedra sinica Stapf (ESP), a traditional Chinese herb, has shown potential in respiratory diseases, but its bioactive components and mechanisms remain unclear. This study investigates the anti-inflammatory effects of ESP-B4, a key ESP-derived compound, in an AR rat model and explores its underlying molecular mechanisms to support novel drug development. An AR rat model was established via ovalbumin (OVA) sensitization. Transcriptome sequencing identified differentially expressed genes associated with ESP-B4 treatment. Nasal mucosal pathology was evaluated using hematoxylin-eosin (HE) staining. The expression levels of TGF-β, Smad3, GATA3, and inflammatory cytokines (IL-5, TNF-α) were measured via RT-qPCR and Western blot. Co-immunoprecipitation (Co-IP) was used to assess Smad3/GATA3 protein interactions. ESP-B4 significantly alleviated AR symptoms, reducing sneezing and nasal scratching frequency. HE staining confirmed improved nasal mucosal integrity with reduced epithelial damage and edema. Mechanistically, ESP-B4 downregulated TGF-β, Smad3, and GATA3 expression while disrupting their protein-protein interaction, leading to suppressed IL-5 and TNF-α levels. ESP-B4 exerts potent anti-inflammatory effects in AR by inhibiting the TGF-β/Smad3/GATA3 signaling axis. These findings highlight its potential as a novel therapeutic agent for AR and provide a scientific basis for further drug development.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147290220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Weighted gene coexpression network analysis and machine learning identify mitochondria programmed cell death-related genes as diagnostic biomarkers for septic shock. WGCNA和机器学习鉴定线粒体程序性细胞死亡相关基因作为感染性休克的诊断生物标志物。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag044

Di Yu, Zhongbin Lai, Jingzhao Xia, Qun Huang, Jin'er Zhang, Shaoyi He

{"title":"Weighted gene coexpression network analysis and machine learning identify mitochondria programmed cell death-related genes as diagnostic biomarkers for septic shock.","authors":"Di Yu, Zhongbin Lai, Jingzhao Xia, Qun Huang, Jin'er Zhang, Shaoyi He","doi":"10.1093/jleuko/qiag044","DOIUrl":"10.1093/jleuko/qiag044","url":null,"abstract":"Septic shock (SS), the most severe stage of sepsis, has a high mortality rate. Mitochondria-mediated programmed cell death (MPCD) plays a key role in SS pathogenesis, but its diagnostic value remains unclear. This study integrated the Gene Expression Omnibus (GEO) public dataset and used the weighted gene coexpression network analysis (WGCNA) method to identify gene modules significantly associated with SS and intersected them with MPCD-related genes to obtain the SS-MPCD gene set. Least absolute shrinkage and selection operator (LASSO) regression and Boruta algorithms screened key genes, with their diagnostic performance verified in an independent queue. Through single-cell transcriptome analysis, immune infiltration score (ssGSEA), and regulatory network construction [transcription factor {TF} microRNA {miRNA}, and protein-protein interaction {PPI}], the immune regulatory characteristics of candidate genes were systematically analyzed. Clinical blood samples were collected, and the expression levels of candidate genes were validated through quantitative real-time polymerase chain reaction (qRT-PCR). Finally, the cecal ligation and puncture (CLP)-induced SS mouse model was used for ACSL1 intervention, and its functional effects were evaluated by survival analysis, hematoxylin and eosin (H&E), qRT-PCR, Western blot (WB), and immunofluorescence (IF). Four diagnostic genes were identified: ACSL1, BLOC1S1, SPTLC2, and TSPO. They were upregulated in SS patients and clinical samples, showed immune cell-specific expression, and were regulated by specific miRNAs/TFs. Immune profiling revealed a neutrophil- and Treg-dominated microenvironment. Inhibiting ACSL1 improved survival, reduced organ damage and inflammation, decreased apoptosis markers, and suppressed neutrophil/Treg infiltration. The study systematically identifies and preliminarily validates 4 MPCD-related diagnostic genes, offering insights into SS pathogenesis and potential early diagnosis.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147574363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Human macrophage phagocytosis of lung cancer cells induced by CD47 blockade is augmented after knockdown of phagocytosis checkpoints mediated by siRNA-loaded lipid nanoparticles. 在sirna负载脂质纳米颗粒介导的吞噬检查点敲低后，CD47阻断诱导的人巨噬细胞对肺癌细胞的吞噬增强。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag043

Kristian W Antonsen, Henriette Mathiesen, Henriette N Friis, Boe S Sorensen, Morten N Andersen, Søren K Moestrup, Anders Etzerodt, Holger J Møller

{"title":"Human macrophage phagocytosis of lung cancer cells induced by CD47 blockade is augmented after knockdown of phagocytosis checkpoints mediated by siRNA-loaded lipid nanoparticles.","authors":"Kristian W Antonsen, Henriette Mathiesen, Henriette N Friis, Boe S Sorensen, Morten N Andersen, Søren K Moestrup, Anders Etzerodt, Holger J Møller","doi":"10.1093/jleuko/qiag043","DOIUrl":"10.1093/jleuko/qiag043","url":null,"abstract":"Macrophages can phagocytose tumor cells. However, tumor cells may avoid phagocytosis by activating macrophage-expressed phagocytosis checkpoints such as SIRPα, LILRB1, or Siglec-10. Here, we investigated whether LNPs loaded with siRNA (siRNA-LNPs), specifically neutralizing these checkpoints, may be used as a counter-regulatory approach to augment cancer cell phagocytosis in human macrophages. The NanoAssemblr Ignite platform was used to prepare siRNA-LNPs targeting genes of interest. Human monocyte-derived macrophages were generated in vitro from healthy anonymous blood donors and treated with one or more siRNA-LNPs under various conditions. Following treatments, the abundance of mRNA was analyzed by RT-qPCR, while membrane protein and soluble protein were measured by flow cytometry and ELISA, respectively. Phagocytosis was assessed by flow cytometry and fluorescence microscopy. Target mRNAs were efficiently downregulated by siRNA-LNPs in a dose-dependent manner. Combination treatment targeting all 3 genes of interest was similar in knockdown effectiveness to a single treatment for each target. A single dose resulted in significant downregulation of mRNA and protein for up to 7 d and did not reduce macrophage viability. Repeated dosing further reduced target abundance. Importantly, we observed a synergy between LILRB1-siRNA-LNPs and CD47 blockade that increased macrophage phagocytosis of NCI-H196 lung cancer cells. In conclusion, transfection with siRNA-LNPs resulted in an efficient simultaneous downregulation of phagocytosis checkpoints in human macrophages and augmented macrophage phagocytosis of tumor cells in response to CD47 blockade in vitro. Using siRNA-LNPs in cancer therapy may be a promising potential approach to augment phagocytosis and the innate immune response against tumor growth.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Re-defining granulomas: bacterial effectors, host circuits, and spatially resolved immunity. 重新定义肉芽肿：细菌效应、宿主电路和空间分解免疫。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag045

Daniel S C Butler

{"title":"Re-defining granulomas: bacterial effectors, host circuits, and spatially resolved immunity.","authors":"Daniel S C Butler","doi":"10.1093/jleuko/qiag045","DOIUrl":"10.1093/jleuko/qiag045","url":null,"abstract":"Granulomas are organized immune aggregates of myeloid and lymphoid cells that arise when the host fails to eliminate persistent stimuli; however, their function remains paradoxical, by promoting both protection from systemic dissemination while also promoting a niche for microbial survival. Traditionally defined by histopathology and morphology, granulomas are now being revisited with high-throughput \"omics approaches. The findings reveal previously unrecognized cellular diversity and cytokine gradients that together shape granuloma behavior. Across diverse pathogens, including Mycobacterium, Salmonella, Yersinia, and Brucella, bacterial effector proteins actively remodel macrophage activation states and cytokine responses to shape granuloma architecture. In parallel, host-driven programs involving IFN-mediated macrophage activation, regulatory cytokine niches, and fibroblast-dependent tissue remodeling establish an immunological landscape in which bacteria operate strategies to survive. Studies of granuloma biology reveal conserved cellular modules that transcend bacterial taxa and mirror features of noninfectious granulomatous inflammation, including iNOS+ core, fibroblast/macrophage cuffs, neutrophil rims, and suppressive macrophage niches. In this review, we integrate these insights to propose a unifying framework in which granulomas represent adaptive but imperfect tissue responses balancing protection and pathology. Understanding how microbial effectors and host immune circuits jointly determine granuloma fate is essential for identifying mechanisms that could be targeted by host-directed strategies to therapeutically reprogram granulomatous inflammation to favor antimicrobial resolution.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Neutrophil biology and fate reprogramming in bacterial infections: mechanisms, plasticity, and therapeutic targeting. 细菌感染中的中性粒细胞生物学和命运重编程：机制、可塑性和治疗靶向。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag033

Asmaa H Mahmoud, Maria A Colombatti Olivieri, John P Bannantine, Gaber S Abdellrazeq

{"title":"Neutrophil biology and fate reprogramming in bacterial infections: mechanisms, plasticity, and therapeutic targeting.","authors":"Asmaa H Mahmoud, Maria A Colombatti Olivieri, John P Bannantine, Gaber S Abdellrazeq","doi":"10.1093/jleuko/qiag033","DOIUrl":"10.1093/jleuko/qiag033","url":null,"abstract":"Neutrophils are essential leukocytes in bacterial infections, with their fate and immune regulation critically shaping disease outcomes. They eliminate pathogens through phagocytosis, degranulation, oxidative burst-mediated killing, and the release of neutrophil extracellular traps (NETs), yet these defenses can also trigger excessive inflammation and tissue damage. Recent advances, including single-cell and spatial transcriptomic profiling, have revealed remarkable neutrophil plasticity and subset heterogeneity, challenging the long-standing view of these cells as short-lived, uniform effectors. This review outlines an integrated framework of neutrophil immunity in bacterial infections, beginning with their development, recruitment, and in situ antimicrobial defense programs. We then examine how neutrophils adapt through immune signaling pathways, effector mechanisms, and fate-determining death programs that actively reshape inflammation and resolution. Within these adaptations, we highlight how host-derived cytokines, lipid mediators, and metabolic cues reprogram neutrophil functions toward either protective antimicrobial roles or pathological tissue-damaging programs. In parallel, bacterial pathogens exploit these same pathways to evade immune clearance. We further detail emerging therapeutic strategies targeting immune checkpoints, signaling nodes, and fate-regulating programs, offering promising avenues to recalibrate neutrophil activity, enhance bacterial control, and reduce immunopathology. To exemplify these principles in vivo, we focus on 2 granulomatous diseases, tuberculosis and paratuberculosis, where neutrophils exhibit context-dependent dysfunctions, including excessive NETosis, metabolic rewiring, and impaired phagocytic clearance. Collectively, these insights position neutrophil fate reprogramming as a central regulatory axis of leukocyte immunity and a tractable target for host-directed therapy in bacterial infections.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Tissue context as a determinant of trained innate immunity: a conserved molecular toolkit with divergent functional outputs. 组织环境作为训练先天免疫的决定因素：具有不同功能输出的保守分子工具包。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiag047

Mary A Oliver, Xenia D Davis, Julia K Bohannon

{"title":"Tissue context as a determinant of trained innate immunity: a conserved molecular toolkit with divergent functional outputs.","authors":"Mary A Oliver, Xenia D Davis, Julia K Bohannon","doi":"10.1093/jleuko/qiag047","DOIUrl":"10.1093/jleuko/qiag047","url":null,"abstract":"Trained innate immunity (TI) challenges the traditional view that adaptive immune cells are solely responsible for establishing immune memory. Instead, innate immune cells can develop a form of memory through persistent epigenetic, metabolic, and antimicrobial modifications, enabling them to respond to secondary challenges in a nonspecific manner. While the molecular mechanisms underlying this trained response have been extensively characterized and are well understood, the intrinsic cellular programs driving trained immunity have not been clearly delineated. Further, the influence of tissue-specific microenvironments remains underexplored. Evidence indicates that the heterogeneity observed in trained immune responses is partly attributable to the functional outcomes shaped by trained immunity within diverse tissue microenvironments, underscoring the complexity and context-dependent nature of this adaptive process. In this review, we explore that TI uses a conserved molecular toolkit whose functional output is dictated by tissue microenvironment. Signals such as oxygen tension, microbiota, local metabolites, cytokine release, and damage-associated molecular patterns can also shape trained innate immunity. The resulting outcomes range from increased antimicrobial defense to maladaptive responses that lead to chronic inflammation and tissue damage. Together, we synthesize findings from hematopoiesis and tissue-resident macrophage biology, emphasizing how immunometabolism and epigenetic mechanisms underpin tissue-specific models of TI. This comprehensive framework resolves contradictions observed across different organs and disease states, positioning tissue instruction as a pivotal determinant of innate immune memory. It demonstrates that trained immunity programs are intricately adapted to tissue niches, with profound implications for infection control, inflammatory diseases, tissue regeneration, and the precise therapeutic targeting of innate immune cells.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13122766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Spatial profiling reveals complex cellular responses of anti-IL5 treatment with mepolizumab in eosinophilic chronic rhinosinusitis with nasal polyposis. 空间分析揭示了mepolizumab抗il - 5治疗嗜酸性慢性鼻窦炎伴鼻息肉病的复杂细胞反应。

IF 3.1 3区医学

Journal of Leukocyte Biology Pub Date : 2026-04-02 DOI: 10.1093/jleuko/qiaf128

Nicholas P West, Sarah M Williams, James Sinclair, Peter Howarth, Peter K Smith, Raquel Alvarado, Peter Earls, Richard J Harvey, Amanda J Cox

{"title":"Spatial profiling reveals complex cellular responses of anti-IL5 treatment with mepolizumab in eosinophilic chronic rhinosinusitis with nasal polyposis.","authors":"Nicholas P West, Sarah M Williams, James Sinclair, Peter Howarth, Peter K Smith, Raquel Alvarado, Peter Earls, Richard J Harvey, Amanda J Cox","doi":"10.1093/jleuko/qiaf128","DOIUrl":"10.1093/jleuko/qiaf128","url":null,"abstract":"There is limited understanding of the impact of anti-IL5 treatment on nasal polyp tissue biology in chronic rhinosinusitis with nasal polyps (CRSwNP). This study examined nasal polyp tissue cellular proteome and transcriptome responses to anti-IL5 treatment in CRSwNP utilizing spatial profiling. GeoMx Digital Spatial Profiling of 80 proteins and 1,833 messenger RNA targets in the polyp stroma and the whole transcriptome (18,815 messenger RNA targets) in polyp epithelia was undertaken on sinonasal biopsies collected from 20 individuals with eosinophilic CRSwNP before and after 16 and 24 wk of mepolizumab treatment. Anti-IL5 therapy in patients with eosinophilic CRSwNP had significant tissue biological impact. Treatment-related changes in polyp stroma proteins associated with checkpoint inhibition (PD-1), neutrophil degranulation (CD6b, CD44, STING1), and the innate immune system (CD14, CD68, STING, CD163) were identified in a protein interaction network. Transcriptionally, there were significant reductions in gene sets associated with the reactome terms \"innate and adaptive immune system,\" \"neutrophil degranulation,\" and \"TGFβ receptor signaling in epithelial-to-mesenchymal transition within polyp stroma,\" as well as \"enhancing antioxidant pathways.\" In polyp epithelia, increases in gene sets associated with the reactome terms \"cilium assembly\" and \"keratinization\" and a reduction in the regulation of KIT signaling were observed. Spatial profiling demonstrates that the effects of anti-IL5 treatment within nasal polyp tissue extend beyond simple eosinophil reduction to regulation of innate and adaptive immune cells and in improving epithelial barrier biology. The clinical relevance of changes to improved barrier function may relate to quality-of-life metrics observed previously with anti-IL5 treatment.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145023459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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