Immunology & Cell Biology最新文献

{"title":"The N6-Methyladenosine-Modified CIT Promotes Uterine Corpus Endometrial Carcinoma Progression by Inhibiting the Hippo Signaling Pathway","authors":"Yuehong Tong,&nbsp;Lili Xu,&nbsp;YiQun Sun,&nbsp;Keke Zhang,&nbsp;Xiaoyan Fu","doi":"10.1111/imcb.70152","DOIUrl":"10.1111/imcb.70152","url":null,"abstract":"<div>\u0000 \u0000 <p>This study investigates the role of CIT gene in uterine corpus endometrial carcinoma (UCEC) progression, focusing on its regulation by m6A methylation. Bioinformatics and experimental analyses (EdU, colony formation assay, Dot blot, MeRIP-PCR, RNA pull-down, qRT-PCR, Western Blotting, apoptosis assay) revealed that CIT was significantly overexpressed in UCEC. Mechanistically, we found that the m6A writer RBM15-mediated CIT mRNA methylation, which was then recognized by the reader IGF2BP1 to enhance CIT mRNA stability and expression. Consequently, this m6A-mediated upregulation of CIT inhibited the Hippo signaling pathway, ultimately suppressing apoptosis and promoting malignant proliferation in UCEC. These findings elucidated a novel RBM15/IGF2BP1-CIT-Hippo axis, providing new theoretical insights and potential therapeutic targets for UCEC.</p>\u0000 </div>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"818-831"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148682876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond the Human Body: Models for Studying Neutrophil Biology","authors":"Salem Hamdan,&nbsp;Malgorzata Wachowska","doi":"10.1111/imcb.70150","DOIUrl":"10.1111/imcb.70150","url":null,"abstract":"<p>Neutrophils are a key component of the immune system, integrating antimicrobial and immunomodulatory functions through various strategies, including phagocytosis, degranulation, generation of reactive oxygen species (ROS), and release of neutrophil extracellular traps (NETs). Owing to their complexity and involvement in a wide range of conditions, including autoimmune diseases, neutrophils have emerged as a major focus of biomedical research. However, it should be noted that neutrophil studies face significant challenges, including short lifespan, terminal differentiation, tendency to spontaneous activation, and donor variability. Moreover, resistance to genetic modifications limits the detailed investigation of gene function and signaling pathways in neutrophil biology. To overcome these constraints, a range of experimental models has been developed. In this review, we present a guide to the currently available neutrophil models (HSPC, iPSC, HL-60, PLB-985, NB4, Kasumi-1, ER-Hoxb8), highlighting their strengths and limitations, with particular emphasis on their value as genetically modifiable platforms. Additionally, we provide an insight into the mechanisms governing neutrophil effector functions.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"771-782"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148576394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Agentic AI for Spatial Omics","authors":"Gianna Pavilion,&nbsp;Cathrine Mbigidde,&nbsp;Rafael Tubelleza,&nbsp;Priya Ramarao-Milne,&nbsp;Arutha Kulasinghe","doi":"10.1111/imcb.70146","DOIUrl":"10.1111/imcb.70146","url":null,"abstract":"<p>This highlight summarises recent advances in agentic artificial intelligence (AI) systems for spatial omics analysis. These systems are compared along two central tensions: autonomy versus accountability, and adaptability versus reproducibility. We argue that progress will depend not on maximising automation, but on defining where autonomy is appropriate.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"736-739"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70146","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148389571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular insights into the anti-inflammatory and antifibrotic effects of licorice–ginger decoction in experimental models of inflammatory arthritis-associated lung fibrosis","authors":"Hui Yuan,&nbsp;Wei Leng,&nbsp;Yanrong Bai,&nbsp;Nan Yu,&nbsp;Yong Yu,&nbsp;Chuangbo Yang,&nbsp;Qian Wu","doi":"10.1111/imcb.70136","DOIUrl":"10.1111/imcb.70136","url":null,"abstract":"<p>Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is a severe autoimmune complication lacking effective treatments. This study investigates the molecular mechanisms underlying the therapeutic effects of licorice–ginger decoction (GGD) in experimental models relevant to arthritis-associated lung fibrosis. Utilizing network pharmacology, transcriptomic sequencing, and molecular docking analyses, we identified the STAT1/ICAM1/IL-17A signaling pathway as crucial for GGD efficacy. Experimental validation in both cellular and murine models demonstrated that GGD markedly alleviated body weight loss, reduced arthritis severity, and improved pulmonary pathological injury under inflammatory arthritis conditions. Mechanistic analyses revealed direct binding of Kae and QR to STAT1/ICAM1, leading to IL-17A inhibition and mitigation of epithelial–mesenchymal transition (EMT) and fibroblast activation. Notably, overexpression of STAT1 attenuated the therapeutic effects of GGD. This study provides mechanistic insights into the anti-inflammatory and antifibrotic effects of GGD in experimental models relevant to arthritis-associated lung fibrosis and offers a potential framework for future mechanistic studies and translational research of classical Chinese formulations.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"794-817"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Emerging Role of UCHL1 in Neurological and Musculoskeletal Diseases","authors":"Ru Feng,&nbsp;Xiu Zhong,&nbsp;Jianjun Li,&nbsp;Adrian A. Achuthan","doi":"10.1111/imcb.70151","DOIUrl":"10.1111/imcb.70151","url":null,"abstract":"<p>Ubiquitin C-terminal hydrolase L1 (UCHL1) is a highly conserved deubiquitinating enzyme that has transitioned from being viewed as a “brain-specific” protein to a global regulator of cellular proteostasis and signal transduction. As a key component of the ubiquitin-proteasome system (UPS), UCHL1 maintains the intracellular free ubiquitin pool through its C-terminal hydrolase activity, while also exhibiting atypical ligase-like functions and acting as a molecular scaffold for signaling complexes. Beyond its classical role in neurons, increasing evidence suggests that UCHL1 participates in diverse pathological conditions including neurodegeneration, cancer, cardiovascular and metabolic diseases, as well as musculoskeletal disorders. Through regulation of protein turnover, oxidative stress, inflammatory signaling, and cell survival, UCHL1 emerges as a context-dependent regulator with dual protective and pathogenic roles. This review explores the sophisticated multi-level regulation of UCHL1, ranging from transcriptional control to epigenetic silencing and posttranslational modifications, summarizes the recent research progress of UCHL1 in various systems, and elaborates on its mechanism of action in various conditions, including neurological and musculoskeletal disorders.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"783-793"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70151","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148667828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ICB Special Feature: Highlights of 2025","authors":"M. Zeeshan Chaudhry","doi":"10.1111/imcb.70149","DOIUrl":"10.1111/imcb.70149","url":null,"abstract":"&lt;p&gt;This special feature brings together a collection of 25 highlight articles curated to bring you up to date on the major leaps in immunology research published over the past year. Driven by single-cell multiomics, advanced spatial imaging, and machine learning, the field has entered a transformative era where immune cell functions are no longer viewed as static, population-averaged signals. Each article in this collection highlights the foundational papers that redefined specific immunology domains in 2025.&lt;/p&gt;&lt;p&gt;The classical view of adaptive immunity is shifting from linear models to fluid, multi-dimensional networks. Rather than a simple, three-signal event, CD8&lt;sup&gt;+&lt;/sup&gt; T cell activation is now recognized as a dynamic journey choreographed across distinct anatomical niches, as highlighted by Borger and Taylor [&lt;span&gt;1&lt;/span&gt;]. Demonstrating a clear affinity for transcriptional control, Chaudhry and Belz [&lt;span&gt;2&lt;/span&gt;] focus on recent studies that reveal that complex multi-state transcription factors dynamically enforce T cell lineage fidelity, balancing immediate effector clearance with the preservation of self-renewing stemness. Bonomi et al. [&lt;span&gt;3&lt;/span&gt;] and Maire and Coquet [&lt;span&gt;4&lt;/span&gt;] highlight how machine learning and generative pipelines now decode the biophysical and mechanical limitations that dictate how a T cell receptor recognizes its antigen. The cellular resolution afforded by single-cell technologies is also revealing the hidden versatility of unconventional T cell lineages. Howson [&lt;span&gt;5&lt;/span&gt;] maps studies showing γδ T cells act as context-dependent surveyors shifting between protection and pathology, while Patton et al. [&lt;span&gt;6&lt;/span&gt;] summarize that macrophages serve as critical antigen presentation hubs that dictate the activation of mucosal-associated invariant T (MAIT) cells via MR1. Dive into these highlights to discover how the latest breakthroughs in single-cell tracking and atomic modeling are fundamentally rewriting the textbook on T cell responses, transcriptional states and antigen recognition.&lt;/p&gt;&lt;p&gt;As our understanding of lymphocyte biology logic deepens, synthetic biology is rapidly evolving from empirical tweaking to rational, computationally guided designing. The race to optimize therapeutic potency is unfolding on multiple fronts. Sek et al. [&lt;span&gt;7&lt;/span&gt;] detail the latest metabolic armoring designed to sustain chimeric antigen receptor (CAR) T cell fitness within hostile tumor microenvironments, ensuring these therapeutic cells run on a full tank before exhaustion kicks in. McLellan et al. [&lt;span&gt;8&lt;/span&gt;] outline a convergence of in vivo lentiviral delivery systems, multiplex CRISPR base editing and de novo antibody generation approaches that bypass cumbersome ex vivo manufacturing entirely. This push for scalable, off-the-shelf therapeutic platforms is redefining natural killer cell-based immunotherapies. Biggi and Souza-Fonseca-Guimaraes [&lt;span&gt;9&lt;/span&gt;] track the translational leap","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"768-770"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Highlights of 2025: Advances in the T-Cell Regulation of Germinal Center Response","authors":"Xinting Zhou,&nbsp;Zhian Chen","doi":"10.1111/imcb.70141","DOIUrl":"10.1111/imcb.70141","url":null,"abstract":"<p>In this 2025 Highlight, we summarize recent advances in T-cell regulation of germinal center (GC) responses. These studies reveal new mechanisms governing follicular helper T (T_FH)-cell function and their control of GC dynamics and B-cell fate decisions, providing insights for rational vaccine design and the prevention of GC dysregulation.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 7","pages":"682-685"},"PeriodicalIF":3.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148262515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics Comes of Age: Immune Profiling of Human Aging","authors":"Kirsten Skye Hicks,&nbsp;Connie Jackaman","doi":"10.1111/imcb.70145","DOIUrl":"10.1111/imcb.70145","url":null,"abstract":"<p>A recent study by Gong et al. maps peripheral immune aging using multi-omic profiling and longitudinal influenza vaccination across adults aged 25–90+, revealing midlife (55–65) immune remodeling. Analyses of PBMCs, proteomics, and cell function show early dysregulation before aging, highlighting links to later disease susceptibility before inflammaging.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 7","pages":"729-731"},"PeriodicalIF":3.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148373972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of Therapeutic Resistance and Recent Advances in Glioblastoma Treatment","authors":"Emerson Achari,&nbsp;Farah Ahmady-Nield,&nbsp;Amit Sharma,&nbsp;Ingo G. H. Schmidt-Wolf,&nbsp;Jarek Maciaczyk,&nbsp;Rodney B. Luwor,&nbsp;Adrian A. Achuthan","doi":"10.1111/imcb.70144","DOIUrl":"10.1111/imcb.70144","url":null,"abstract":"<p>High-grade central nervous system cancers incur a significant burden of care on society. The combination of therapeutic resistance and high mortality makes it both a challenging target and a devastating diagnosis. Of these, one in two is characterized as glioblastoma (GBM) with a median survival rate of only 13.5 months with the current standard of therapy. Modern interventions, such as PD-1 and CTLA-4 checkpoint inhibition and autologous CAR T cell delivery, remain stymied by both the difficult nature of drug delivery to the brain and the inherent immunosuppressive tumor microenvironment. However, recent advances in the characterization of GBM have unveiled promising new therapeutic avenues aiming to target and eliminate the tumor. In this review, we summarize the mechanisms through which GBM is initiated, localized, and eludes therapy responses and provide an update on recent advances made within this therapeutic space to overcome GBM-mediated immunosuppression. We also discuss the challenges with current and next generational treatment strategies before finally exploring the landscape of potential future therapeutic targets.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 7","pages":"711-728"},"PeriodicalIF":3.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70144","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148374002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel adaptor protein, ARAP, orchestrates Fcγ receptor signaling in mouse dendritic cells via Rap1 activation and NF-κB-mediated cytokine production","authors":"Chohee Park,&nbsp;Mi Jin Yu,&nbsp;Jong Ran Lee","doi":"10.1111/imcb.70133","DOIUrl":"10.1111/imcb.70133","url":null,"abstract":"<p>Fcγ receptors (FcγRs), key mediators of antibody-dependent immune responses, are critical for dendritic cell (DC) activation and adaptive immunity initiation. Although the general importance of FcγR signaling is well established, the specific intracellular pathways remain insufficiently defined. ARAP (activation-dependent, raft-recruited ADAP-like phosphoprotein) is a novel adaptor protein identified in T-cell receptor signaling pathways. ARAP is expressed across various tissues and cell types, including DCs. To address the functional significance of ARAP, homologous recombination was performed to generate mice with an <i>ARAP</i> deficiency. In this study, we investigated the role of ARAP in FcγR-mediated DC function using <i>ARAP</i>-deficient mice. The results revealed that bone marrow-derived DCs from <i>ARAP</i>-deficient mice exhibited defects in FcγR-mediated proximal signaling and integrin-mediated adhesion. In addition, <i>ARAP</i>-deficient DCs exhibited reduced nuclear translocation of NF-κB p65 and decreased production of inflammatory cytokines. These findings establish ARAP as a selective and critical regulator of FcγR signaling, suggesting FcγR involvement in dendritic cell Rap1-mediated adhesion and NF-κB-dependent cytokine responses.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 7","pages":"642-655"},"PeriodicalIF":3.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70133","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148012856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}