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Interleukin-12: Central Roles in Immune Regulation and Disease Therapy. 白细胞介素-12:在免疫调节和疾病治疗中的核心作用。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-30 DOI: 10.1111/imcb.70167
Anthi Psoma, Geert van den Bogaart
{"title":"Interleukin-12: Central Roles in Immune Regulation and Disease Therapy.","authors":"Anthi Psoma, Geert van den Bogaart","doi":"10.1111/imcb.70167","DOIUrl":"https://doi.org/10.1111/imcb.70167","url":null,"abstract":"<p><p>Interleukin-12 (IL-12) is a key immunoregulatory cytokine produced primarily by antigen-presenting cells. During infection, IL-12 orchestrates innate immune responses and shapes the nature of subsequent adaptive immunity. Specifically, by promoting interferon-γ (IFN-γ) production in helper and cytolytic T cells and natural killer (NK) cells, it promotes the activation of these cells and drives the differentiation of CD4<sup>+</sup> T cells into type 1 T helper (Th1) cells. IL-12 is a heterodimeric cytokine composed of the p35 and p40 subunits, whose coordinated expression is required for formation of the bioactive p70 molecule. The promiscuous use of these subunits within the IL-12 cytokine family, where p40 and p35 also pair with other partners to form IL-23, IL-27, and IL-35, creates structural and functional overlap that enables fine-tuned immune regulation. Given its potent immune functions, it is not surprising that IL-12 availability is regulated at multiple levels, including gene transcription, subunit assembly, and shared receptor signaling components. In this review, we provide an overview of IL-12, how it is produced and secreted and its mechanisms of action. We also discuss the targeting of IL-12 for the treatment of various diseases, including bacterial infections, autoimmune diseases, and cancer.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079131","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}
引用次数: 0
Think BIG, Stay Connected: A Regional Immunology Meeting as a Durable Model for Scientific Community Building. 思考大,保持联系:区域免疫学会议作为科学社区建设的持久模式。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-29 DOI: 10.1111/imcb.70165
Danielle I Stanisic, Rajiv Khanna, Severine Navarro, J Alejandro Lopez
{"title":"Think BIG, Stay Connected: A Regional Immunology Meeting as a Durable Model for Scientific Community Building.","authors":"Danielle I Stanisic, Rajiv Khanna, Severine Navarro, J Alejandro Lopez","doi":"10.1111/imcb.70165","DOIUrl":"https://doi.org/10.1111/imcb.70165","url":null,"abstract":"<p><p>Regional scientific meetings occupy a distinctive but underexamined position within the research ecosystem. Smaller and more accessible than national congresses, yet broader in scope than institutional seminar programm, they provide opportunities for repeated interactions across institutions, career stages, and research domains. The Brisbane Immunology Group (BIG) meeting is one of the longest-running and most influential regional meetings associated with the Australian and New Zealand Society for Immunology (ASI), providing a focal point for immunology researchers across Queensland, Australia, and beyond. This article examines the BIG meeting as a case study of a regional immunology community that has sustained scientific engagement, mentoring, and collaboration for 25 years. Drawing on historical records and thematic analysis of interviews with organizers, senior contributors, and recent attendees, we identify six characteristics that have contributed to the longevity and impact of the meeting: accessibility, cross-institutional ownership, intergenerational participation, social integration, programmatic continuity with adaptive innovation, and deliberate recognition of community contributions. We argue that BIG functions not merely as an annual scientific meeting but as a regional community of practice that supports scientific collaboration, professional identity formation, and leadership development. The BIG experience provides broader lessons regarding the role of regional meetings in strengthening scientific communities, supporting future scientific leaders and sustaining disciplinary vitality.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079086","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}
引用次数: 0
Advances in Cytosolic dsRNA Sensing of Viral Infections. 病毒感染细胞质dsRNA检测的研究进展。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-27 DOI: 10.1111/imcb.70163
Sofia Maceratessi, Natalia G Sampaio
{"title":"Advances in Cytosolic dsRNA Sensing of Viral Infections.","authors":"Sofia Maceratessi, Natalia G Sampaio","doi":"10.1111/imcb.70163","DOIUrl":"https://doi.org/10.1111/imcb.70163","url":null,"abstract":"<p><p>Detection of abnormal RNA species, such as dsRNA, in the cell cytoplasm underscores innate immune response to viral infections. In humans, the cytosolic dsRNA sensors include RLRs (RIG-I, MDA5, and LGP2), PKR, and OASs (OAS1, OAS2, OAS3, and OASL). These receptors are all known to bind varying forms of dsRNA and activate differential signaling pathways whose outcome is to limit viral replication. In this article, we describe some of the major recent advances in dsRNA sensing of viral infections, such as the role of endogenous host RNAs in activating sensors, phase separation as a new layer of sensor regulation, cell type-specific versus universal pathway regulation mechanisms, and the interplay between these pathways within the cell. We have focused on key discoveries of the past 2 years, mainly in mammalian systems.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149068738","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}
引用次数: 0
Unmasking the Influence of Viral Micro-RNAs on Host Immunity. 揭示病毒微rna对宿主免疫的影响。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-22 DOI: 10.1111/imcb.70164
Riley J K Easton, Bernadette M Saunders
{"title":"Unmasking the Influence of Viral Micro-RNAs on Host Immunity.","authors":"Riley J K Easton, Bernadette M Saunders","doi":"10.1111/imcb.70164","DOIUrl":"https://doi.org/10.1111/imcb.70164","url":null,"abstract":"<p><p>Micro-RNAs (miRNAs) are key regulators of human immunity, controlling critical cellular programmes including proliferation, differentiation, apoptosis, and immune activation to shape the host response to infection. Multiple human-infecting viruses encode their own miRNA (v-miRNA), enabling them to co-opt host gene regulatory machinery to subvert immunity, establish persistence and evade immune-mediated killing. This review synthesizes the current evidence on viral miRNAs and their roles in host-virus interactions, with an explicit focus on immune regulation. We examine how different viruses use v-miRNAs to modulate core immune functions, including antigen presentation, cytokine signaling, NK and CD8 T-cell activation, and apoptosis. We also examine how v-miRNAs manipulate viral gene expression to aid immune evasion and promote persistence. Particular emphasis is placed on experimentally validated immune targets and their clinical consequences. Collectively, these examples illustrate the convergent evolution of v-miRNA-mediated immune evasion across diverse viral families. Understanding this class of molecules will provide insight into critical immune evasion strategies employed by clinically important viruses and may identify novel targets for diagnostic and antiviral therapeutics, including antagomir-based and RNA silencing approaches.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149014927","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}
引用次数: 0
Hypercapnia Induces Mitochondrial Adaptations and Alters Glutamine Metabolism to Drive a Distinct Metabolic Phenotype in Monocytes. 高碳酸血症诱导线粒体适应并改变谷氨酰胺代谢以驱动单核细胞的独特代谢表型。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-16 DOI: 10.1111/imcb.70162
Ben Reddan, David E Phelan, Xiaofei Yin, Lorraine Brennan, Martina Wallace, Eoin P Cummins
{"title":"Hypercapnia Induces Mitochondrial Adaptations and Alters Glutamine Metabolism to Drive a Distinct Metabolic Phenotype in Monocytes.","authors":"Ben Reddan, David E Phelan, Xiaofei Yin, Lorraine Brennan, Martina Wallace, Eoin P Cummins","doi":"10.1111/imcb.70162","DOIUrl":"https://doi.org/10.1111/imcb.70162","url":null,"abstract":"<p><p>Carbon dioxide (CO<sub>2</sub>) is an ancient and ubiquitous physiological gas generated during aerobic respiration. Historically viewed as a simple metabolic waste product, CO<sub>2</sub> has received far less research attention than oxygen (O<sub>2</sub>), the primary substrate of aerobic respiration. However, emerging evidence has revealed important roles for CO<sub>2</sub> in immunometabolism, immunology, muscle physiology, and clinical medicine. While circulating pCO<sub>2</sub> levels are tightly regulated, patients with lung diseases such as chronic obstructive pulmonary disease (COPD) frequently develop hypercapnia, pCO<sub>2</sub> > 45 mmHg. Hypercapnia is associated with significantly increased mortality, higher risk of ICU admission, and a global prevalence estimated at 13-15 million patients. Its broader clinical consequences remain poorly understood and are inadequately integrated into current therapeutic paradigms. Here, we examined the impact of hypercapnia on the metabolic profile of monocytes. We demonstrate that 24 h of buffered hypercapnia induces a marked reduction in mitochondrial mass. This is accompanied by dysregulation of mitochondrial membrane potential and key bioenergetic substrates (NADH/NAD<sup>+</sup> and ATP content). We further show that hypercapnia alters the abundance of metabolites and proteins associated with mitochondrial metabolism, with effects spanning glucose, glutamine, and lipid metabolism. Thus, we provide direct mechanistic evidence that hypercapnia directly alters the glutamine-glutamate-proline synthesis axis. Collectively, these findings establish the foundation for a discrete hypercapnic metabolic phenotype, that is, in several respects, distinct from the metabolic adaptations observed in hypoxia. We propose that hypercapnia triggers a cascade of metabolic adaptations with tissue-dependent consequences on cellular effector functions.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148981797","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}
引用次数: 0
Role of T Cells in Chronic Pain: Mechanisms, Regulation, and Therapeutic Implications. T细胞在慢性疼痛中的作用:机制、调节和治疗意义。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-06 DOI: 10.1111/imcb.70160
Yuanyuan Li, Ruihan Yang, Shipeng Wei, Jing Wang, Haoyu Ke, Wenguo Fan
{"title":"Role of T Cells in Chronic Pain: Mechanisms, Regulation, and Therapeutic Implications.","authors":"Yuanyuan Li, Ruihan Yang, Shipeng Wei, Jing Wang, Haoyu Ke, Wenguo Fan","doi":"10.1111/imcb.70160","DOIUrl":"https://doi.org/10.1111/imcb.70160","url":null,"abstract":"<p><p>T cells are critical for controlling the adaptive immune response and maintaining the homeostasis of the body. Recent evidence suggests that T cells are involved in the initiation, maintenance, and resolution of chronic pain by releasing mediators such as cytokines and endogenous opioids. In this review, we highlight recent advances in the involvement of T cells in chronic pain. We also describe how T cells act on sensory neurons to promote, suppress, or even resolve pain. Finally, we review how T cells are regulated and how we can translate these findings to develop therapies for chronic pain.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148899945","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}
引用次数: 0
Carbocisteine Reduces Airway Mucus Obstruction and Alters Inflammatory Cell Populations in a Model of Muco-Obstructive Lung Disease 卡西汀减少气道粘液阻塞和改变粘膜阻塞性肺疾病模型中的炎症细胞群。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-04 Epub Date: 2026-08-13 DOI: 10.1111/imcb.70156
Peter Ferris, Ryan Brown, Michael McKelvey, Daniel F. McAuley, Marcus A. Mall, Bronwen Connolly, Clifford C. Taggart
{"title":"Carbocisteine Reduces Airway Mucus Obstruction and Alters Inflammatory Cell Populations in a Model of Muco-Obstructive Lung Disease","authors":"Peter Ferris,&nbsp;Ryan Brown,&nbsp;Michael McKelvey,&nbsp;Daniel F. McAuley,&nbsp;Marcus A. Mall,&nbsp;Bronwen Connolly,&nbsp;Clifford C. Taggart","doi":"10.1111/imcb.70156","DOIUrl":"10.1111/imcb.70156","url":null,"abstract":"<p>Muco-obstructive lung diseases, including chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and bronchiectasis, are characterized by excessive mucus production, airway surface dehydration, impaired mucociliary clearance, and progressive lung function decline. As the efficacy of current therapies often declines with muco-obstructive disease progression, contributing significantly to morbidity and mortality, there is a need for improved treatments that address underlying defects in mucus homeostasis and airway physiology. In this study, we evaluate the effects of carbocisteine, a mucoactive therapeutic, in the βENaC-transgenic (βENaC-Tg) model of muco-obstructive lung disease. Short-term carbocisteine administration significantly reduced airway mucus obstruction, potentially through decreased concentrations of Muc5ac and Muc5b. Notably, carbocisteine treatment modulated key inducers of mucus production, such as interleukin (IL)-13 and the upstream promoter cytokine IL-17, suggesting broader effects on mucoregulatory pathways. Carbocisteine administration was observed to alter mononuclear cell populations, impacting specific inflammatory subsets of CD11b alveolar macrophages and Ly6c monocytes, indicating immunomodulatory effects, either directly or secondary to improved mucus clearance. However, despite changes in immune cell populations, short-term administration failed to mitigate lung damage and inflammation associated with established muco-obstructive lung disease. These findings demonstrate the potent mucoactive effect of carbocisteine in established muco-obstructive lung disease, through a broader mechanism of action than previously understood, with the potential to modulate inflammatory responses for preventive or long-term treatment strategies.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"833-844"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70156","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148756975","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}
引用次数: 0
BLIMP-1 and CD39 expression define human effector memory regulatory T cells in blood and recall responses to viruses BLIMP-1和CD39的表达决定了血液中人类效应记忆调节性T细胞和对病毒的回忆反应。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-04 Epub Date: 2026-07-14 DOI: 10.1111/imcb.70148
Chansavath Phetsouphanh, Laura Cook, Katherine J. L. Jackson, Deirdre Cuff, Vera Klemm, Bikash Manandhar, Denise C. Hsu, Yin Xu, John J. Zaunders, Anthony D. Kelleher, Nabila Seddiki
{"title":"BLIMP-1 and CD39 expression define human effector memory regulatory T cells in blood and recall responses to viruses","authors":"Chansavath Phetsouphanh,&nbsp;Laura Cook,&nbsp;Katherine J. L. Jackson,&nbsp;Deirdre Cuff,&nbsp;Vera Klemm,&nbsp;Bikash Manandhar,&nbsp;Denise C. Hsu,&nbsp;Yin Xu,&nbsp;John J. Zaunders,&nbsp;Anthony D. Kelleher,&nbsp;Nabila Seddiki","doi":"10.1111/imcb.70148","DOIUrl":"10.1111/imcb.70148","url":null,"abstract":"<p>BLIMP-1, a transcriptional repressor initially identified in plasma B-cell differentiation, also regulates CD8<sup>+</sup> T cells and is differentially expressed between naïve and effector/memory CD4<sup>+</sup> T cells. However, the functions of BLIMP-1 in human CD4<sup>+</sup> regulatory T cells (Tregs) remain unclear. We found BLIMP-1 mRNA levels were low in naïve Tregs from thymus and cord blood, but high in effector/memory Tregs from adult peripheral blood. We confirmed the expression of BLIMP-1 mRNA by microarray of healthy T-cell populations and single-cell RNA-sequencing of SARS-CoV-2 spike-specific CD4<sup>+</sup> T cells from convalescent COVID-19 patients. We found activated memory Tregs expressed the highest levels of BLIMP-1, FOXP3, and CD39 transcripts and protein. We show that CD39<sup>+</sup> Tregs, regardless of in vitro or in vivo activation, had the highest levels of BLIMP-1 protein expression and significantly more IL-10 mRNA than CD39<sup>neg</sup> cells. The same result was found through reanalysis of public single cell RNA-sequencing data from lung (tissue and lymph node) SARS-CoV-2 spike-specific Tregs, where cells with high levels of BLIMP-1 mRNA had significantly more IL-10 mRNA than cells with low BLIMP-1 mRNA. Single-cell RNA-sequencing identified an extended transcriptomic profile of these CD39<sup>+</sup> Tregs that includes the genes encoding HPGD, CTLA-4, HELIOS, TIGIT, CXCR6, CCR8, and GARP. Together, these data indicate that both circulating and lung resident effector memory Tregs maintain a conserved phenotype following stimulation by cognate antigen. Our data provide further insight into the functions and potential therapeutic targets of the large regulatory T-cell component of CD4<sup>+</sup> T-cell responses to pathogens.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"757-767"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70148","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148443484","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}
引用次数: 0
Mast Cells Selectively Deliver Extracellular Vesicle-Encapsulated mRNA to Colorectal Cancer Cells 肥大细胞选择性地向结直肠癌细胞传递细胞外囊泡包封mRNA。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-04 Epub Date: 2026-07-06 DOI: 10.1111/imcb.70147
Rosie Lanzloth, Bader El Farran, Ram Podicheti, Douglas B. Rusch, Heather M. O'Hagan
{"title":"Mast Cells Selectively Deliver Extracellular Vesicle-Encapsulated mRNA to Colorectal Cancer Cells","authors":"Rosie Lanzloth,&nbsp;Bader El Farran,&nbsp;Ram Podicheti,&nbsp;Douglas B. Rusch,&nbsp;Heather M. O'Hagan","doi":"10.1111/imcb.70147","DOIUrl":"10.1111/imcb.70147","url":null,"abstract":"<p>Mast cells (MCs), a type of granulocytic immune cell, exert contrasting effects on tumorigenesis. The anti- or pro-tumorigenic activity of MCs depends on the cancer type, tumor microenvironment, and MC localization within the tumor. Consequently, their role remains controversial and poorly understood across multiple cancer types, including colorectal cancer (CRC). Most proposed mechanisms underlying MC activity in CRC have focused on MC secretion of biological factors. In this study, we demonstrated that MCs transfer extracellular vesicles containing mRNAs and proteins to CRC cells. This process occurs through a tightly regulated mechanism that requires direct cell–cell contact, calcium signaling, and integrin-mediated interactions. Such requirements resemble aspects of immunological synapses observed between lymphocytes and cancer cells. The novel mode of intercellular communication between MCs and cancer cells described here may help refine our understanding of MC functions in cancer biology.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":"740-756"},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70147","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148395411","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}
引用次数: 0
Correction to “Differential peritoneal resident macrophage depletion and omental milky spot disruption after high versus low clodronate-loaded liposome dose treatment” 更正“高剂量与低剂量氯膦酸脂质体治疗后腹膜巨噬细胞消耗和大网膜乳斑破坏的差异”。
IF 3.3 4区 医学
Immunology & Cell Biology Pub Date : 2026-09-04 Epub Date: 2026-08-12 DOI: 10.1111/imcb.70154
{"title":"Correction to “Differential peritoneal resident macrophage depletion and omental milky spot disruption after high versus low clodronate-loaded liposome dose treatment”","authors":"","doi":"10.1111/imcb.70154","DOIUrl":"10.1111/imcb.70154","url":null,"abstract":"<p>\u0000 <span>M. Ferriz</span>, <span>N. Álvarez-Ladrón</span>, <span>A. Gutiérrez-González</span>, <span>M. H. Fernández-Sesma</span>, <span>A. Starešinčić</span>, and <span>C. Ardavín</span>, “ <span>Differential Peritoneal Resident Macrophage Depletion and Omental Milky Spot Disruption After High Versus Low Clodronate-Loaded Liposome Dose Treatment</span>,<i>”</i> <i>Immunology &amp; Cell Biology</i> <span>104</span>, no. <span>2</span> (<span>2026</span>): <span>139</span>–<span>149</span>, https://doi.org/10.1111/imcb.70077\u0000 </p><p>In the originally published version of this article, one of the affiliations for author Alejandra Gutiérrez-González was inadvertently omitted.</p><p>The missing affiliation is:</p><p>Universidad Alfonso X el Sabio (UAX), Facultad de Ciencias Biomédicas y de la Salud, Avenida de la Universidad 1, Madrid, Spain.</p><p>The corrected author and affiliation list is as follows:</p><p>Margarita Ferriz<sup>1,a</sup>, Natalia Álvarez-Ladrón<sup>1,2,a</sup>, Alejandra Gutiérrez-González<sup>1,3,a</sup>, Marta H. Fernández-Sesma<sup>1,a</sup>, Ana Starešinčić<sup>1</sup> and Carlos Ardavín<sup>1</sup></p><p><sup>1</sup> Department of Immunology and Oncology, National Center for Biotechnology/CSIC, Darwin 3, 28049 Madrid, Spain.</p><p><sup>2</sup> Escuela de Doctorado, Universidad Autónoma de Madrid; 28048 Madrid, Spain</p><p><sup>3</sup> Universidad Alfonso X el Sabio (UAX), Facultad de Ciencias Biomédicas y de la Salud, Avenida de la Universidad 1, Madrid, Spain.</p><p>The online version of this article has been corrected accordingly.</p>","PeriodicalId":179,"journal":{"name":"Immunology & Cell Biology","volume":"104 8","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imcb.70154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148710587","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}
引用次数: 0
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