Experimental hematology最新文献

{"title":"Editorial for the SI: Stem cells and angiogenesis","authors":"Nobuyuki Takakura MD & PhD","doi":"10.1016/j.exphem.2025.104865","DOIUrl":"10.1016/j.exphem.2025.104865","url":null,"abstract":"","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"149 ","pages":"Article 104865"},"PeriodicalIF":2.1,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144863698","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":"IFC Editorial Board","authors":"","doi":"10.1016/S0301-472X(25)00159-6","DOIUrl":"10.1016/S0301-472X(25)00159-6","url":null,"abstract":"","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"149 ","pages":"Article 104868"},"PeriodicalIF":2.1,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144863697","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":"Ontogenetic drivers of neutrophil heterogeneity","authors":"Ali Hageb ,&nbsp;Merieme Farjia ,&nbsp;Collins Osei-Sarpong ,&nbsp;Carlos Silvestre-Roig","doi":"10.1016/j.exphem.2025.104863","DOIUrl":"10.1016/j.exphem.2025.104863","url":null,"abstract":"<div><div>Neutrophil development is a tightly regulated, multistep process involving stem cell commitment, differentiation, and maturation in the bone marrow. Chromatin remodeling, transcriptional networks, epigenetic reprogramming, metabolic adaptations, and structural changes collectively govern neutrophil production, shaping both maturation states and functional potential. Although these processes can be leveraged to adapt the neutrophil pool quantitatively and qualitatively during homeostasis or inflammatory stress, their dysregulation often drives disease progression. In this review, we examine how these ontogenetic factors specify neutrophil functions and underscore the significance of functional diversity across different maturation states.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"151 ","pages":"Article 104863"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144798605","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 myeloid transcription factor Elf1 regulates genes with function in innate immunity.","authors":"Prabha Varghese, Maria-Paz Garcia-Cuellar, Robert K Slany","doi":"10.1016/j.exphem.2025.104864","DOIUrl":"10.1016/j.exphem.2025.104864","url":null,"abstract":"<p><p>Transcription factor networks are critical hubs for organ development. Here, we investigated the hematopoietic function of the E-twenty six (Ets)-family transcription factor E74-like factor 1 (Elf1) that is normally predominantly expressed in monocytes. Strikingly, Elf1 was not only a direct downstream target of homeobox A9 (HoxA9) and leukemogenic mixed-lineage leukemia (MLL) fusion proteins but it was also consistently overexpressed in acute myeloid leukemia (AML) regardless of the underlying genotypic alteration. Chromatin immunoprecipitation localized Elf1 to archetypical myeloid enhancers and promoters as defined by colocalization with HoxA9 and Meis1. In perturbation/ectopic expression experiments Elf1 controlled a characteristic transcriptional program dominated by genes with a function in innate immunity. Importantly, in functional assays Elf1 was crucial for the rapid transcriptional response of myeloid cells toward lipopolysaccharide as demonstrated by upregulation of NfkB and RelB. This activity could be assigned to genomic control elements that bound Elf1 in vitro and in vivo and it was confirmed in myelocytes with a genetic knockout of Elf1. These results give insight into the architecture of the common hematopoietic enhancer where redundant binding of transcription factors may be explained by special requirements that appear only under certain conditions.</p>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":" ","pages":"104864"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803952","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":"ZC3H13 facilitates the progression of acute myeloid leukemia through m6A-FOXP1-mediated metabolic reprogramming","authors":"Jiaheng Wang,&nbsp;Linjuan Xu,&nbsp;Gang Wang,&nbsp;Wenping Wu,&nbsp;Hongwei Kong","doi":"10.1016/j.exphem.2025.104862","DOIUrl":"10.1016/j.exphem.2025.104862","url":null,"abstract":"<div><div>Acute myeloid leukemia (AML) is a complex hematologic malignancy characterized by rapid progression and high relapse rates. Zinc finger CCCH domain-containing protein 13 (ZC3H13) has been implicated in the pathogenesis of various diseases, but its role in AML remains unclear. This study aimed to elucidate the function and underlying mechanisms of ZC3H13 in AML. Gene expression patterns and correlations with patient survival were analyzed using the Gene Expression Profiling Interactive Analysis (GEPIA) database. ZC3H13 expression was quantified in AML bone marrow samples and cell lines via real-time reverse-transcription PCR (qRT-PCR) and Western blotting. Cell proliferation was assessed using Cell counting kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (EdU) assays, whereas flow cytometry was employed to evaluate cell cycle progression, apoptosis, and reactive oxygen species (ROS) levels. Glycolytic activity—including glucose consumption, lactate production, and ATP levels—was measured using commercial kits. Oxidative stress markers such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) were also quantified. The LinkedOmics database was used to identify ZC3H13-associated genes and predict their functional correlations. Potential m6A modification sites on FOXP1 mRNA were predicted using the SRAMP tool and validated through methylated RNA immunoprecipitation (MeRIP) assays. A dual-luciferase reporter assay confirmed direct binding of ZC3H13 to the FOXP1 promoter. ZC3H13 was found to be highly expressed in AML bone marrow and cell lines. Functionally, ZC3H13 promoted cell proliferation, enhanced glycolysis, and suppressed both apoptosis and oxidative stress. Mechanistically, ZC3H13 stabilized FOXP1 expression via m6A methylation, thereby contributing to AML progression. In conclusion, ZC3H13 accelerates AML development by modulating the m6A-FOXP1 axis, leading to metabolic reprogramming. These findings provide novel insights into AML pathogenesis and offer potential targets for therapeutic intervention.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"151 ","pages":"Article 104862"},"PeriodicalIF":2.1,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144803953","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":"A-to-I RNA editing in hematologic immunity and malignancy","authors":"Wei Liang Gan ,&nbsp;Leilei Chen","doi":"10.1016/j.exphem.2025.104861","DOIUrl":"10.1016/j.exphem.2025.104861","url":null,"abstract":"<div><div>Blood cells exhibit a profound relationship with RNA editing, particularly adenosine deaminase acting on RNA 1 (ADAR1)-dependent adenosine-to-inosine (A-to-I) RNA editing, impacting immune cell activity, hematologic malignancy, and ultimately determining the efficacy of treatment options such as immune checkpoint inhibitors (ICIs). This review highlights the myriad roles A-to-I RNA editing plays in leukocytes, with particular focus on its regulation of immune cell development and maturation, and how its dysregulation contributes to malignant hematopoiesis. With the growing implementation of ICIs as cancer therapeutics, it is imperative to take stock of our understanding of A-to-I RNA editing in immune cells to improve cancer treatment modalities.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"150 ","pages":"Article 104861"},"PeriodicalIF":2.1,"publicationDate":"2025-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144752761","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":"IFC Editorial Board","authors":"","doi":"10.1016/S0301-472X(25)00139-0","DOIUrl":"10.1016/S0301-472X(25)00139-0","url":null,"abstract":"","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"148 ","pages":"Article 104848"},"PeriodicalIF":2.5,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144703937","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":"Fetal lymphocyte progenitors efficiently generate innate-like B cells but make a more limited contribution to the production of conventional lymphocytes","authors":"Encarnacion Montecino-Rodriguez,&nbsp;Kenneth Dorshkind","doi":"10.1016/j.exphem.2025.104860","DOIUrl":"10.1016/j.exphem.2025.104860","url":null,"abstract":"<div><div>Various progenitor populations with lymphoid potential emerge in multiple waves of fetal development and can do so independent from hematopoietic stem cells (HSCs). This review compares and contrasts data from our analysis of a mutant mouse in which fetal but not adult lymphopoiesis is intact with results from lineage tracing studies. This allowed us to address how efficiently and how long fetal lymphoid progenitors generated lymphoid progeny after birth. We then present, based on the data in these reports, a working model proposing that fetal lymphocyte progenitors efficiently generate innate-like B-1 and marginal zone B cells, but their contribution to the production of B and T cells of the adaptive immune system is more limited. Instead, lymphocyte development from adult HSCs is necessary to fill secondary lymphoid tissues with conventional lymphocytes, and fetal progenitors lack the potential to do so. We propose that, in addition to generating innate-like effectors, the key role of fetal lymphoid progenitors is to produce a sufficient number of B and T cell progeny, particularly in the intestines, so that the newborn and neonate have functional immunity until lymphopoiesis from HSCs is fully established.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"150 ","pages":"Article 104860"},"PeriodicalIF":2.1,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717828","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":"Impaired CMV-specific CD4+ T-cell reconstitution is associated with CMV infection after letermovir cessation","authors":"Luxiang Wang ,&nbsp;Su Li ,&nbsp;Jiayu Huang ,&nbsp;Zilu Zhang ,&nbsp;Zengkai Pan ,&nbsp;Chuanhe Jiang ,&nbsp;Haiyang Lu ,&nbsp;Sujiang Zhang ,&nbsp;Yang Cao ,&nbsp;Xiaohong Cai ,&nbsp;Gang Cai ,&nbsp;Xiaoxia Hu","doi":"10.1016/j.exphem.2025.104859","DOIUrl":"10.1016/j.exphem.2025.104859","url":null,"abstract":"<div><div>Cytomegalovirus (CMV) is a prevalent virus that causes substantial morbidity and mortality in allogeneic hematopoietic stem cell transplantation (allo-HSCT). Although letermovir (LTV) prophylaxis has revolutionized CMV management, clinically significant CMV infection (cs-CMVi) after letermovir cessation presents a new challenge. Effective CMV control is heavily dependent on the reconstitution of CMV-specific cell-mediated immunity (CMI); however, there is a lack of reliable immunologic biomarkers for identifying cs-CMVi after LTV withdrawal. The aim of the present study was to determine how different CMV preventive regimens and cs-CMVi impacted CMV-CMI reconstitution and the risk factors for late-onset cs-CMVi after LTV cessation. The patients were divided into the preemptive therapy (PET, <em>n</em> = 55) and LTV (<em>n</em> = 23) groups. LTV was significantly more effective at decreasing the cumulative incidence of cs-CMVi than PET (4.3% vs. 65.4%, <em>p</em> &lt; 0.01) within 100 days post-allo-HSCT. Meanwhile, after day 100, the cumulative incidence of late-onset cs-CMVi was higher in the LTV than in the PET group (26.1% vs. 7.3%, <em>p</em> = 0.02). We found that LTV delayed the reconstitution of CMV-specific CD8⁺ T cells. Patients who experienced cs-CMVi had lower CMV-specific interferon (IFN)-γ⁺CD4⁺ T-cell counts than those who did not develop cs-CMVi. Patients with CMV disease had the lowest numbers of CMV-specific polyfunctional CD4⁺ T cells. Polyfunctional CMV-specific CD4⁺ T-cell count &lt; 2.01 cells/µL might predict late-onset cs-CMVi after LTV cessation (50.0% vs. 7.69%, <em>p</em> = 0.04). Our findings establish an association between CMV prophylaxis, cs-CMVi, and CMV-specific T-cell response reconstitution post-allo-HSCT.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"150 ","pages":"Article 104859"},"PeriodicalIF":2.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667458","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":"Fetal heart as a new local site for hematopoiesis and macrophage formation","authors":"Norika Liu ,&nbsp;Haruko Nakano ,&nbsp;Atsushi Nakano","doi":"10.1016/j.exphem.2025.104818","DOIUrl":"10.1016/j.exphem.2025.104818","url":null,"abstract":"<div><div>Cardiac tissue macrophages are crucial components of the immune system and tissue homeostasis. Traditionally, these macrophages have been classified into three primary lineages: yolk sac blood island-derived erythromyeloid progenitor (EMP), yolk sac hemogenic endothelial-derived late-EMP, and hematopoietic stem cell (HSC)-derived macrophages. These classifications have shaped our understanding of the developmental origin of macrophages in the heart. However, recent studies have significantly shifted this perspective by revealing that the heart itself possesses an intrinsic source of macrophages, independent of the traditionally recognized hematopoietic sources. This discovery has added a new dimension to our understanding of macrophage biology in the context of cardiac development. Our recent work has provided compelling evidence that endocardial cells exhibit hematopoietic potential during embryonic days (E) 8.5 to E10. This discovery challenges the previously held belief that macrophages in the heart are exclusively derived from EMP or HSC. Endocardial cells give rise to a distinct population of cardiac tissue macrophages that play vital roles in heart morphogenesis. These findings open up new avenues for understanding how macrophages contribute to heart formation, homeostasis, and their disruption. This review summarized the latest findings on the role of endocardium-derived macrophages, along with other macrophage lineages, in contributing to heart development and the maintenance of cardiac homeostasis.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"149 ","pages":"Article 104818"},"PeriodicalIF":2.5,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567355","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}