European Journal of Immunology最新文献

Plasmodium berghei Radiation-Attenuated Sporozoite-Immunized Mice Require Infectious Sporozoite Challenge to Maintain Protective Immunity 伯氏疟原虫辐射减毒孢子子免疫小鼠需要感染性孢子子刺激来维持保护性免疫

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-25 DOI: 10.1002/eji.202451542

Hardik Patel, Naveen Yadav, Rajesh Parmar, Vishakha Bhurani, Aditi Mathur, Dolly Jagwani, Avantika Ahiya, Dillip K. Behera, Urszula Krzych, Sarat K. Dalai

{"title":"Plasmodium berghei Radiation-Attenuated Sporozoite-Immunized Mice Require Infectious Sporozoite Challenge to Maintain Protective Immunity","authors":"Hardik Patel, Naveen Yadav, Rajesh Parmar, Vishakha Bhurani, Aditi Mathur, Dolly Jagwani, Avantika Ahiya, Dillip K. Behera, Urszula Krzych, Sarat K. Dalai","doi":"10.1002/eji.202451542","DOIUrl":"https://doi.org/10.1002/eji.202451542","url":null,"abstract":"<div>\u0000 \u0000 Plasmodium radiation-attenuated sporozoites (RAS) confer sterile protection in mammalian hosts. The duration of protection is affected by the dose of RAS, the route of immunization, and the timing of primary challenge (PC). Giving PC shortly after the last Plasmodium berghei (Pb) RAS immunization of C75BL/6 mice led to the long-term sterile protection, whereas delaying PC beyond 6 months resulted in parasitemia. The mechanisms responsible for the divergent outcome remain unknown. Because liver effector/memory CD8+T cells are associated with lasting protection, herein we asked if any functions of CD8+T cells would be diminished or lost by delaying PC. Using the Pb protection model, we characterized functional attributes and phenotypes of liver and spleen CD8+T cells following early and delayed PC. Compared with CD8+T cells before the challenge, liver KLRG-1intCD107+ and IFN-γ+IL-2+CD8+T cells increased after early but decreased following delayed PC. Memory CD8+T cells exhibited higher expression of Bcl-2 at early rather than delayed PC. Finally, splenic and liver-draining lymph node CD8+T cells expressed significantly higher CXCR6 and the respective ligands but only following early PC. Collectively, our results show that enhanced proliferation, migration, and elevated effector functions of CD8+T cells are associated with the longevity of sterile protection in the Pb RAS murine model.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875597","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

Differential Induction of Endoplasmic Reticulum Stress Signaling by Antibody Isotypes: Implications for Plasma Cell Differentiation 抗体同型诱导内质网应激信号的差异：对浆细胞分化的影响

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-25 DOI: 10.1002/eji.202451428

Kunie Obayashi, Tomomitsu Doi, Kazuhiro Sumida, Motoyoshi Endo

引用次数: 0

Distinct HLA Haplotypes Are Associated With an Altered Strength of SARS-CoV-2-Specific T-Cell Responses and Unfavorable Disease Courses 不同的HLA单倍型与sars - cov -2特异性t细胞反应强度的改变和不利的疾病病程相关

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-21 DOI: 10.1002/eji.202451497

C. Dörnte, A. Datsi, V. Traska, J. Kostyra, M. Wagner, O. Brauns, C. Lamsfuß, H. Winkels, V. Balz, J. Enczmann, O. Adams, L. Mueller, H. Baurmann, B. Eiz-Vesper, A. Bonifacius, R. V. Sorg, C. Dose, J. Schmitz, A. Richter, J. Fischer, M. Schuster

{"title":"Distinct HLA Haplotypes Are Associated With an Altered Strength of SARS-CoV-2-Specific T-Cell Responses and Unfavorable Disease Courses","authors":"C. Dörnte, A. Datsi, V. Traska, J. Kostyra, M. Wagner, O. Brauns, C. Lamsfuß, H. Winkels, V. Balz, J. Enczmann, O. Adams, L. Mueller, H. Baurmann, B. Eiz-Vesper, A. Bonifacius, R. V. Sorg, C. Dose, J. Schmitz, A. Richter, J. Fischer, M. Schuster","doi":"10.1002/eji.202451497","DOIUrl":"https://doi.org/10.1002/eji.202451497","url":null,"abstract":"Infection with SARS-CoV-2 results in mild to severe COVID-19 disease courses. Several studies showed the association of impaired T-cell responses and certain HLA haplotypes with disease severity. However, it remained unclear if T-cell activation was compromised due to a general reduction of presented epitopes or other intrinsic factors within APCs or T cells. Furthermore, a potential reduction of presented epitopes would suggest if an upcoming SARS-CoV-2 variant could escape T-cell immunity. Hence, knowledge about the T-cell epitope landscape of SARS-CoV-2 would allow to better understand mechanisms leading to severe disease and to estimate the potential stability of the T-cell response in light of virus evolution, which might provide insights for future vaccine designs. Hence, in the present study, the T-cell epitope landscape of SARS-CoV-2 was determined via in vitro T-cell stimulation plus in silico prediction. HLAs associated with mild and severe disease courses showed almost the same potential in epitope presentation, suggesting intrinsic factors of APCs or T cells as contributors to the more severe disease courses. As T-cell epitopes did also not originate from regions of SARS-CoV-2 having shown high mutation rates in the past, a relatively stable T-cell response can be expected regarding new SARS-CoV-2 strains in the future. Analysis of the T-cell epitope landscape of SARS-CoV-2 suggests T-cell intrinsic factors as likely modulators of disease severity and that the capacity of MHC-peptide presentation remains stable among circulating SARS-CoV-2 viral strains.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451497","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856845","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

Gluten-Free Diet Induces Small-Scale Changes Across Multiple T-Cell Subsets in NOD Mice 无麸质饮食诱导NOD小鼠多个t细胞亚群的小规模变化

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-21 DOI: 10.1002/eji.202451559

Veronika Niederlova, Juraj Michalik, Barbora Drabonova, Radka Cisarova, David Funda, Ondrej Stepanek

{"title":"Gluten-Free Diet Induces Small-Scale Changes Across Multiple T-Cell Subsets in NOD Mice","authors":"Veronika Niederlova, Juraj Michalik, Barbora Drabonova, Radka Cisarova, David Funda, Ondrej Stepanek","doi":"10.1002/eji.202451559","DOIUrl":"https://doi.org/10.1002/eji.202451559","url":null,"abstract":"Nonobese diabetic (NOD) mice are a widely used animal model to study mechanisms leading to autoimmune diabetes. A gluten-free diet reduces and delays the incidence of diabetes in NOD mice, but the underlying mechanisms remain largely unknown. In this study, we performed single-cell transcriptomic and flow cytometry analysis of T cells and innate lymphocytes in the spleen and pancreatic lymph nodes of NOD mice fed a gluten-free or standard diet. We observed that the gluten-free diet did not induce a substantial alteration in the abundance or phenotype of any lymphocyte subset that would directly explain its protective effect against diabetes. However, the gluten-free diet induced subtle changes in the differentiation of subsets with previously proposed protective roles in diabetes development, such as Tregs, activated γδT cells, and NKT cells. Globally, the gluten-free diet paradoxically promoted activation and effector differentiation across multiple subpopulations and induced genes regulated by IL-2, IL-7, and IL-15. In contrast, the standard diet induced type I interferon-responsive genes. Overall, the gluten-free diet might prevent diabetes in NOD mice by inducing small-scale changes in multiple cell types rather than acting on a specific lymphocyte subset.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451559","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143852665","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

Pamidronate-Induced Clinical Remission in Chronic Non-bacterial Osteomyelitis Is Associated with Reduced Vγ9Vδ2 T-Cell Receptor Expression 帕米膦酸钠诱导的慢性非细菌性骨髓炎临床缓解与Vγ9Vδ2 t细胞受体表达降低相关

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-21 DOI: 10.1002/eji.202451609

Lily Watson, Athimalaipet V Ramanan, Elizabeth Oliver, Francisca Segers, Gareth W. Jones, Christine Chew, Anu Goenka

引用次数: 0

Maternal Administration of Probiotics Augments IL17-Committed γδ T Cells in the Newborn Lung 母体给予益生菌增加新生儿肺中il - 17承诺的γδ T细胞

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-21 DOI: 10.1002/eji.202451051

Yohannes Tafesse, Arnaud Köhler, Guillem Sanchez Sanchez, Patricia Brito Rodrigues, Marko Verce, Panagiotis Vitsos, Isoline Verdebout, Moosa Rezwani, Maria Papadopoulou, Amandine Everard, Véronique Flamand, David Vermijlen

{"title":"Maternal Administration of Probiotics Augments IL17-Committed γδ T Cells in the Newborn Lung","authors":"Yohannes Tafesse, Arnaud Köhler, Guillem Sanchez Sanchez, Patricia Brito Rodrigues, Marko Verce, Panagiotis Vitsos, Isoline Verdebout, Moosa Rezwani, Maria Papadopoulou, Amandine Everard, Véronique Flamand, David Vermijlen","doi":"10.1002/eji.202451051","DOIUrl":"https://doi.org/10.1002/eji.202451051","url":null,"abstract":"<div>\u0000 \u0000 The early life period is increasingly being recognized as a window of opportunity to shape immunity, where microbiota and related probiotics have an important impact. Innate γδ T cells are the first T cells generated in utero, populating epithelial tissues such as the lung and contributing to tissue protection through, for example, IL17 production. Here, we studied the influence of maternal microbiota and probiotic supplementation during pregnancy on innate γδ T cells in the lung and thymus of newborn mice. Detailed time-kinetic experiments showed that at birth, the murine lung T cell population was specifically dominated by IL17-committed γδ T cells expressing an invariant Vγ6Vδ1 TCR. Single-cell RNA-sequencing showed that the biased IL17-commitment of perinatal lung γδT cells is highly conserved between mice and humans. While maternal microbiota depletion with antibiotics tended to decrease the frequency of the lung Vγ6 T cells of the offspring at birth, the maternal administration of Lacticaseibacillus rhamnosus (L.rhm.), but not of Bifidobacterium animalis subsp. lactis (B.lac.), increased significantly their frequency, resulting in the augmentation of the IL17-commitment of the mouse lung T cell compartment. Altogether, our data indicate that the maternal microbiota contributes to the shaping of IL17-committed γδT cells in the lungs of newborns and that maternal administration of specific probiotic strains can enhance this process.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856844","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

Updating the Discontinuity Theory to the Extended Immunity: The Symmunobiome Concept 从不连续理论到扩展免疫的更新：共生群落概念

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-19 DOI: 10.1002/eji.202451528

Federico Boem, Ingrid Lamminpää, Amedeo Amedei

{"title":"Updating the Discontinuity Theory to the Extended Immunity: The Symmunobiome Concept","authors":"Federico Boem, Ingrid Lamminpää, Amedeo Amedei","doi":"10.1002/eji.202451528","DOIUrl":"https://doi.org/10.1002/eji.202451528","url":null,"abstract":"The immune system (IS) is commonly understood as a system composed of specific cells and tissues that have evolved to contrast pathogens and defend the host. By virtue of this capacity, it has come to be considered capable of making an essential distinction, that between self versus non-self, which would contribute to a clear identity of the organism. However, in the wake of evolution and ecology, growing evidence suggests that the so-called immune system, which also evolved from symbiotic interactions with external agents, is not just a defensive system that merely protects the organism but, on the contrary, is involved in many global regulatory and homeostatic functions. Moreover, in performing these many functions, IS is not only an ensemble of host cells and tissues but functionally is constitutively determined by the interaction with a set of associated microorganisms, that is, the human microbiome. In this scenario, it is open-and-shut that the microbiome itself is a functional part of this extended immune system. Organisms and microbiomes together, therefore, form a functional whole, which constitutes a privileged form of biological organization. In light of this evidence showing the inadequacy of traditional accounts, we propose to extend and supplement the current IS conceptualization by introducing the notion of the symmunobiome. With this term, we intend to characterize the microbiome's own and unavoidable component to overall immune functionality. Therefore, we suggest a new immune system determination, articulated in three linked pillars—adaptive immunity, innate immunity, and symmunobiome—to better grasp the diverse functionality of extended immunity.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451528","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849103","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

Dimethyl Fumarate Negatively Regulates MYC Signaling and Promotes Cell-Cycle Arrest in T-Cells through a GSH-Dependent Mechanism 富马酸二甲酯通过gsh依赖机制负调控MYC信号传导并促进t细胞细胞周期阻滞

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-19 DOI: 10.1002/eji.202451399

Kazuya Sato, Shin-ichiro Kawaguchi, Junko Izawa, Takashi Ikeda, Kiyomi Mashima, Norihito Takayama, Hiroko Hayakawa, Kaoru Tominaga, Hitoshi Endo, Yoshinobu Kanda

{"title":"Dimethyl Fumarate Negatively Regulates MYC Signaling and Promotes Cell-Cycle Arrest in T-Cells through a GSH-Dependent Mechanism","authors":"Kazuya Sato, Shin-ichiro Kawaguchi, Junko Izawa, Takashi Ikeda, Kiyomi Mashima, Norihito Takayama, Hiroko Hayakawa, Kaoru Tominaga, Hitoshi Endo, Yoshinobu Kanda","doi":"10.1002/eji.202451399","DOIUrl":"https://doi.org/10.1002/eji.202451399","url":null,"abstract":"<div>\u0000 \u0000 Recent evidence indicates that the TCA cycle metabolite fumarate plays a specific role in modulating signaling pathways in immune cells. We have previously shown that dimethyl fumarate (DMF) reduces glutathione (GSH) activity and causes the accumulation of cellular reactive oxygen species (ROS), thereby compromising effector immune responses and metabolic activities in activated T-cells. However, the precise mechanism by which DMF modulates T-cell signaling pathways remains to be elucidated. This study demonstrates that DMF inhibits T-cell proliferation, independent of T-cell receptor (TCR) engagement, and this response is fully reversible by replenishing GSH. Immunoblot analysis showed that DMF had different impacts on TCR downstream signaling by decreasing MYC expression while promoting the phosphorylation of Akt and Erk1/2. Cell cycle analysis demonstrated that exposure to DMF led to negative regulation of cell cycle-related proteins and induced T-cells into G0/G1 arrest, which was also rescued by antioxidants. Several genes related to GSH synthesis were upregulated at the same time, suggesting that a potential compensatory response may occur to reduce oxidative burst following DMF treatment. Our results suggest that DMF-mediated oxidative stress alters a range of cell signaling pathways, including MYC, leading to cell cycle arrest and a defective proliferative response of T-cells during activation.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849079","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 IL-6-Producing B Cells Promote the Differentiation of Monocytes Toward an Anti-Inflammatory CD16⁺CD163⁺CD206⁺PD-L1⁺ Phenotype in Tuberculosis 人il -6生成B细胞促进单核细胞向抗炎CD16 + CD163 + CD206 + PD-L1 +结核表型分化

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-19 DOI: 10.1002/eji.202451509

Alan Bénard, Luciana Balboa, Maxime Caouaille, Lea Ravon-Katossky, Etienne Meunier, Simon Fillatreau, Maria Del Carmen Sasiain, Olivier Neyrolles, Denis Hudrisier

{"title":"Human IL-6-Producing B Cells Promote the Differentiation of Monocytes Toward an Anti-Inflammatory CD16⁺CD163⁺CD206⁺PD-L1⁺ Phenotype in Tuberculosis","authors":"Alan Bénard, Luciana Balboa, Maxime Caouaille, Lea Ravon-Katossky, Etienne Meunier, Simon Fillatreau, Maria Del Carmen Sasiain, Olivier Neyrolles, Denis Hudrisier","doi":"10.1002/eji.202451509","DOIUrl":"https://doi.org/10.1002/eji.202451509","url":null,"abstract":"<div>\u0000 \u0000 The polarization of the monocyte/macrophage compartment toward an anti-inflammatory profile is considered detrimental in tuberculosis (TB), but the factors controlling M2 polarization in this context are still poorly understood. Here, we found that B cells promote the differentiation of human monocytes toward an M2-like activation program through a process primarily dependent on IL-6 and the activation of STAT3 signaling in monocytes. This confers monocytes with immunomodulatory properties characterized by a reduced ability to produce proinflammatory cytokines and to stimulate IFNγ secretion by allogeneic T cells. Our findings were validated using B cells from TB patients, which constitutively produce high levels of IL-6, underscoring the clinical relevance of our experimental observations. Collectively, our results indicate that human B-cell-derived IL-6 might impair TB immunity by driving monocyte polarization toward an anti-inflammatory phenotype.\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143849080","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

Combined Deletion of ZFP36L1 and ZFP36L2 Drives Superior Cytokine Production in T Cells at the Cost of Cell Fitness ZFP36L1和ZFP36L2的联合缺失以牺牲细胞适应性为代价驱动T细胞中更好的细胞因子产生

IF 4.5 3区医学

European Journal of Immunology Pub Date : 2025-04-18 DOI: 10.1002/eji.202451641

Nordin D. Zandhuis, Antonia Bradarić, Carmen van der Zwaan, Arie J. Hoogendijk, Branka Popović, Monika C. Wolkers

{"title":"Combined Deletion of ZFP36L1 and ZFP36L2 Drives Superior Cytokine Production in T Cells at the Cost of Cell Fitness","authors":"Nordin D. Zandhuis, Antonia Bradarić, Carmen van der Zwaan, Arie J. Hoogendijk, Branka Popović, Monika C. Wolkers","doi":"10.1002/eji.202451641","DOIUrl":"https://doi.org/10.1002/eji.202451641","url":null,"abstract":"A key feature of cytotoxic CD8+ T cells for eliminating pathogens and malignant cells is their capacity to produce proinflammatory cytokines, which include TNF and IFNγ. Provided that these cytokines are highly toxic, a tight control of their production is imperative. RNA-binding proteins (RBPs) are essential for the fine-tuning of cytokine production. The role of the RBP ZFP36L1 and its sister protein ZFP36L2 herein has been established, but their relative contribution to cytokine production is not well understood. We here compared the effect of ZFP36L1 and ZFP36L2 single and double deficiency in murine effector CD8+ T cells. Whereas single deficient T cells significantly increased cytokine production, double deficiency completely unleashed the cytokine production. Not only the TNF production was substantially prolonged in double-deficient T cells. Also, the production of IFNγ reached unprecedented levels with >90% IFNγ-producing T cells compared with 3% in WT T cells after 3 days of continuous activation. This continuous cytokine production by double-deficient T cells was also observed in tumor-infiltrating lymphocytes in vivo, however, with no effect on tumor growth. ZFP36L1 and ZFP36L2 double deficiency resulted in decreased cell viability, impaired STAT5 signaling, and dysregulated cell cycle progression. In conclusion, while combined deletion in ZFP36L1 and ZFP36L2 can drive continuous cytokine production even upon chronic activation, safeguards are in place to counteract such super-cytokine producers.","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 4","pages":""},"PeriodicalIF":4.5,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451641","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143845868","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