ImmunityPub Date : 2025-07-02DOI: 10.1016/j.immuni.2025.06.002
Benjamin A. Devlin, Dang M. Nguyen, Diogo Ribeiro, Gabriel Grullon, Madeline J. Clark, Amelie Finn, Alexis M. Ceasrine, Seneca Oxendine, Martha Deja, Ashka Shah, Shomik Ati, Anne Schaefer, Staci D. Bilbo
{"title":"Excitatory-neuron-derived interleukin-34 supports cortical developmental microglia function","authors":"Benjamin A. Devlin, Dang M. Nguyen, Diogo Ribeiro, Gabriel Grullon, Madeline J. Clark, Amelie Finn, Alexis M. Ceasrine, Seneca Oxendine, Martha Deja, Ashka Shah, Shomik Ati, Anne Schaefer, Staci D. Bilbo","doi":"10.1016/j.immuni.2025.06.002","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.002","url":null,"abstract":"Neuron-microglia interactions dictate the development of neuronal circuits in the brain. However, the factors that regulate these processes across development are largely unknown. Here, we found that interleukin-34 (IL-34), a neuron-derived cytokine, was upregulated in early development and maintained neuroprotective, mature microglia in the anterior cingulate cortex (ACC) of mice. IL-34 expression increases in the second week of post-natal life and was primarily produced by excitatory neurons. Excitatory-neuron-specific deletion of IL-34 reduced microglia numbers and microglial TMEM119 expression and increased aberrant microglial phagocytosis of excitatory thalamocortical synapses in the ACC. Acute, low-dose blocking of IL-34 at post-natal day 15 similarly decreased microglial TMEM119 and aberrantly increased microglial phagocytosis of synapses. Viral overexpression of IL-34 induced TMEM119 expression and prevented appropriate microglial phagocytosis of synapses. These findings establish IL-34 as a key regulator of neuron-microglia crosstalk in post-natal brain development, controlling both microglial maturation and synapse engulfment.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"647 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144533905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-30DOI: 10.1016/j.immuni.2025.06.010
Chirag H. Patel, Jonathan D. Powell
{"title":"More TOR: The expanding role of mTOR in regulating immune responses","authors":"Chirag H. Patel, Jonathan D. Powell","doi":"10.1016/j.immuni.2025.06.010","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.010","url":null,"abstract":"The mammalian/mechanistic target of rapamycin (mTOR) is an evolutionarily conserved multi-node signaling pathway that integrates critical environmental cues to control cellular growth. Decades worth of studies have intricately dissected the mTOR pathway to identify regulatory signals that are essential for regulating immune cell activation, differentiation, and function. As the mTOR field continues to evolve, so too does our understanding of these new findings in immune cells. Our group and others have previously reviewed the role of mTOR in regulating specific immune responses. Here, we provide an updated review of our current understanding of mTOR’s comprehensive role in immune cell biology. In addition, we offer emerging ideas and areas of investigation where mTOR might be further explored and impactfully targeted to improve overall human health given mTOR’s prominent role in aging and cancer.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"39 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144516235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-30DOI: 10.1016/j.immuni.2025.06.005
Dig B. Mahat, Heena Kumra, Sarah A. Castro, Emily Metcalf, Kim Nguyen, Ryo Morisue, William W. Ho, Ivy Chen, Brandon Sullivan, Leon H. Yim, Arundeep Singh, Jiayu Fu, Sean K. Waterton, Yu-Chi Cheng, Enrico Moiso, Vikash P. Chauhan, Hernandez Moura Silva, Stefani Spranger, Rakesh K. Jain, Phillip A. Sharp
{"title":"Mutant p53 exploits enhancers to elevate immunosuppressive chemokine expression and impair immune checkpoint inhibitors in pancreatic cancer","authors":"Dig B. Mahat, Heena Kumra, Sarah A. Castro, Emily Metcalf, Kim Nguyen, Ryo Morisue, William W. Ho, Ivy Chen, Brandon Sullivan, Leon H. Yim, Arundeep Singh, Jiayu Fu, Sean K. Waterton, Yu-Chi Cheng, Enrico Moiso, Vikash P. Chauhan, Hernandez Moura Silva, Stefani Spranger, Rakesh K. Jain, Phillip A. Sharp","doi":"10.1016/j.immuni.2025.06.005","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.005","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer characterized by activating <em>KRAS</em> mutations and <em>TP53</em> alterations. <em>TP53</em> missense mutations lose their wild-type tumor-suppressor function. Here, we studied whether p53 missense mutations have potential gain-of-function oncogenic roles and their impact on cancer-cell-intrinsic gene expression and the tumor immune microenvironment (TME) in PDAC. p53<sup>R172H</sup> established an immunosuppressive TME and impaired the efficacy of immune checkpoint inhibitors (ICIs) by regulating a distinct set of chemokines. Among these, tumor-specific reduction of <em>Cxcl1</em>, which encodes a chemoattractant for neutrophils, promoted T cell infiltration and decreased tumor growth. Mechanistically, p53<sup>R172H</sup> occupied the distal enhancers of <em>Cxcl1</em> and amplified its expression. These enhancers were responsible for <em>Cxcl1</em> expression and were essential for its immunosuppressive function. Nuclear factor κB (NF-κB) was a critical cofactor required for p53<sup>R172H</sup> occupancy at these enhancers. Thus, a common mutation in a tumor-suppressor transcription factor appropriates enhancers, thereby stimulating chemokine expression and establishing an immunosuppressive TME that diminishes ICI efficacy in PDAC.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"46 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144516214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-30DOI: 10.1016/j.immuni.2025.06.006
Megan L. Clark, Kamen P. Simeonov, Walter K. Mowel, Michaël F. Michieletto, Leonel Joannas, Jasmine M. Wright, Isabel Erickson, Lexus R. Johnson, Rakesh Krishnan, César de la Fuente-Núñez, Andy J. Minn, Jorge Henao-Mejia
{"title":"Mitochondrial complex IV remodeling in tumor-associated macrophages amplifies interferon signaling and promotes anti-tumor immunity","authors":"Megan L. Clark, Kamen P. Simeonov, Walter K. Mowel, Michaël F. Michieletto, Leonel Joannas, Jasmine M. Wright, Isabel Erickson, Lexus R. Johnson, Rakesh Krishnan, César de la Fuente-Núñez, Andy J. Minn, Jorge Henao-Mejia","doi":"10.1016/j.immuni.2025.06.006","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.006","url":null,"abstract":"Tumor-associated macrophages (TAMs) influence tumor progression and immune checkpoint blockade (ICB) efficacy. Interferon (IFN)-TAMs predict better survival and ICB responses, yet the mechanisms governing IFN-TAMs remain unclear. Here, we identify NDUFA4, a complex IV subunit of the electron transport chain, as a functional switch controlling TAM function and anti-tumor immunity. NDUFA4 expression sustained pro-tumoral TAMs. However, intratumoral IFNs decreased NDUFA4 expression in TAMs via the cooperative action of NDUFA4L3 and <em>miR-147</em>, co-encoded by a conserved bifunctional transcript. Mechanistically, NDUFA4 repression increased mitochondrial DNA release into the cytoplasm and subsequent STING activation, thereby amplifying anti-tumor IFN-induced transcriptional programs in TAMs. Finally, we designed RNA-based therapeutics that leveraged the specificity of <em>miR-147</em> for the <em>Ndufa4</em> transcript to enhance ICB efficacy and inhibit B16 melanoma tumor growth. These findings uncover mitochondrial complex IV remodeling as a critical mechanism governing the functional adaptation of macrophages to distinct microenvironments with broad implications for immunotherapy.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"10 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144516213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-27DOI: 10.1016/j.immuni.2025.06.003
Guoqi Li, Congcong Zhang, Yang Li, Jie Yang, Jianing Wu, Yihui Shao, Ke Ma, Xinyu Zhang, Shuolin Zhu, Jie Du, Xin-Liang Ma, Liping Wang, Zhuofeng Lin, Ping Li, Yulin Li
{"title":"Optogenetic vagal nerve stimulation attenuates heart failure by limiting the generation f monocyte-derived inflammatory CCRL2+ macrophages","authors":"Guoqi Li, Congcong Zhang, Yang Li, Jie Yang, Jianing Wu, Yihui Shao, Ke Ma, Xinyu Zhang, Shuolin Zhu, Jie Du, Xin-Liang Ma, Liping Wang, Zhuofeng Lin, Ping Li, Yulin Li","doi":"10.1016/j.immuni.2025.06.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.003","url":null,"abstract":"Parasympathetic neuronal dysfunction is associated with heart failure (HF), yet the underlying mechanism is poorly understood. Here, we report that targeted vagal nerve stimulation (VNS) using optogenetics attenuated cardiac remodeling and HF induced by pressure overload. Unbiased approaches revealed that VNS decreased the proportion of Ccrl2<sup>+</sup> macrophages, which were derived from myeloid monocytes and exhibited a distinct tumor necrosis factor alpha (TNF-α) cytokine-responsive, pro-hypertrophic, and profibrotic signature. Elimination of Ccrl2<sup>+</sup> macrophages prevented cardiac remodeling and HF. Ccrl2<sup>+</sup>-macrophage-specific overexpression or global genetic loss of α7 nicotinic acetylcholine receptor (α7nAChR) highlighted their crucial contribution to VNS-mediated cardioprotection. Activation of α7nAChR inhibited Ccrl2<sup>+</sup> macrophages’ TNF-α responsiveness through increased expression of the transcription factor NRF2. Cardiac Ccrl2<sup>+</sup> macrophages and TNF-α-responsive proteins positively correlated with cardiac remodeling and dysfunction in humans. An α7nAChR agonist effectively blocked the development of HF. These results suggest that the vagal neuroimmune axis modulates HF and is a promising target for treatment.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"47 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144516236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-26DOI: 10.1016/j.immuni.2025.05.024
Catherine Mooser, Francesca Ronchi, Julien P. Limenitakis, Cristina Kalbermatter, Sandro Christensen, Mercedes Gomez de Agüero, Tobias Fuhrer, Uwe Sauer, Andrew J. Macpherson, Stephanie C. Ganal-Vonarburg
{"title":"Diet-derived LPS determines intestinal IgA induction and repertoire characteristics independently of the microbiota","authors":"Catherine Mooser, Francesca Ronchi, Julien P. Limenitakis, Cristina Kalbermatter, Sandro Christensen, Mercedes Gomez de Agüero, Tobias Fuhrer, Uwe Sauer, Andrew J. Macpherson, Stephanie C. Ganal-Vonarburg","doi":"10.1016/j.immuni.2025.05.024","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.024","url":null,"abstract":"A hallmark of the main secreted antibody immunoglobulin A (IgA) is its mutational load that accumulates throughout life. Although this is mainly interpreted in terms of continuing microbial induction, we show that dietary composition during early life can promote IgA induction, its repertoire, and mutational diversification independently of microbial exposure. Using germ-free and colonized mice fed different diets formulated with proprietary grain-based processing or from purified chemicals with different principal macronutrient calorie sources, we found that dietary lipopolysaccharide contamination led to Toll-like receptor (TLR) 4 signaling and promoted germinal center activity in the intestinal immune compartment. The effects of lipopolysaccharide on mucosal immune induction were phenocopied only when presented within colloidal liposomes rather than in dispersed solution. These findings indicate that dietary composition and its formulation can leave a durable impression on the resultant IgA repertoire.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"58 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144488377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-25DOI: 10.1016/j.immuni.2025.06.004
Erin Janssen, Mrinmoy Das, Jordan Butts, Mohammed Alasharee, Saikat Mukherjee, Gabriel L. Lozano, Chitong Rao, Andrew F. Livingston, Brian Woods, Emma Smith, Zachary Peters, Elena Milin, Maria A. Beamer, Hazel Wilkie, Juan-Manuel Leyva-Castillo, Christy Kam, Ali Sobh, Majed Dasouki, Rima Hanna Wakim, Ghassan Dbaibo, Raif S. Geha
{"title":"DOCK8 in T cells promotes Th17 and Treg cell functionality to restrain mucosal mast cells and limit susceptibility to oral anaphylaxis","authors":"Erin Janssen, Mrinmoy Das, Jordan Butts, Mohammed Alasharee, Saikat Mukherjee, Gabriel L. Lozano, Chitong Rao, Andrew F. Livingston, Brian Woods, Emma Smith, Zachary Peters, Elena Milin, Maria A. Beamer, Hazel Wilkie, Juan-Manuel Leyva-Castillo, Christy Kam, Ali Sobh, Majed Dasouki, Rima Hanna Wakim, Ghassan Dbaibo, Raif S. Geha","doi":"10.1016/j.immuni.2025.06.004","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.06.004","url":null,"abstract":"Immunoglobulin E (IgE)-mediated release of mediators from mast cells (MCs) drives food allergy, and intestinal MC load is an important determinant of disease severity. Dedicator of cytokinesis 8 (DOCK8)-deficient patients are highly susceptible to food allergy. We found that they exhibited elevated serum MC tryptase levels, suggesting increased MC load. <em>Dock8</em><sup>−/−</sup> mice also had exaggerated IgE-mediated oral anaphylaxis, expansion of jejunal mucosal MCs (MMCs), and elevated serum levels of MMC-derived tryptase. This resulted in increased intestinal permeability, which promoted antigen absorption and thereby oral anaphylaxis. Mechanistically, these events were driven by an intestinal cascade in which reduced interleukin (IL)-17 cytokines led to dysbiosis, which drove IL-25 production. Increased IL-25 enhanced T helper (Th)2 production of IL-4 that expanded MMCs and exaggerated oral anaphylaxis. Furthermore, the failure of DOCK8-deficient T regulatory (Treg) cells to suppress intestinal IL-4 production and MC expansion left the exaggerated anaphylaxis unrestrained. These results suggest multi-faceted coordination between the microbiome, mucosal T cells, and MCs to restrict oral anaphylaxis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"37 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144479515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-25DOI: 10.1016/j.immuni.2025.05.025
Verena van der Heide, Gabriel Laghlali, Bennett Davenport, Beatrice Cubitt, Vladimir Roudko, Daniel Choo, Kevin Jhun, Etienne Humblin, Abishek Vaidya, Krista Angeliadis, Travis Dawson, Glaucia Furtado, Alice O. Kamphorst, Michael Schotsaert, Rafi Ahmed, Juan Carlos de la Torre, Dirk Homann
{"title":"Prolonged but finite antigen presentation promotes reversible defects of “helpless” memory CD8+ T cells","authors":"Verena van der Heide, Gabriel Laghlali, Bennett Davenport, Beatrice Cubitt, Vladimir Roudko, Daniel Choo, Kevin Jhun, Etienne Humblin, Abishek Vaidya, Krista Angeliadis, Travis Dawson, Glaucia Furtado, Alice O. Kamphorst, Michael Schotsaert, Rafi Ahmed, Juan Carlos de la Torre, Dirk Homann","doi":"10.1016/j.immuni.2025.05.025","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.025","url":null,"abstract":"Generation of functional memory CD8<sup>+</sup> T cells typically requires engagement of CD4<sup>+</sup> T cells. In certain acutely resolving infections, however, effector and memory CD8<sup>+</sup> T (Tmem) cell formation appears impervious to the lack of CD4<sup>+</sup> T cell help. Nevertheless, “helpless” CD8<sup>+</sup> Tmem cells may respond poorly upon rechallenge. The origin and long-term fate of helpless CD8<sup>+</sup> Tmem cells remain incompletely understood. Using multiple host-pathogen systems, we demonstrate that helpless effector CD8<sup>+</sup> T cell differentiation was largely normal, with a paradoxical accumulation of TCF1<sup>hi</sup> “memory precursors.” However, exposure of CD8<sup>+</sup> T cells to residual antigen impaired the development of the Tmem pool. These defects eventually resolved over time, with full restoration of memory potential and recall capacity. Our findings identify prolonged antigen presentation under helpless conditions as an essential determinant for transient CD8<sup>+</sup> Tmem cell dysfunction in acutely resolving infections and highlight plasticity within the Tmem compartment, with implications for vaccination strategies and beyond.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"7 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144479514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ImmunityPub Date : 2025-06-23DOI: 10.1016/j.immuni.2025.05.026
Leonardo F. Jurado, Andrew W. Daman, Ziyi Li, Vanessa M.S. Ross, Kristina Nikolaou, Kim A. Tran, Oleg Loutochin, Victor A. McPherson, Renaud Prével, Raquel Tarancón, Katalina Couto, Erwan Pernet, Nargis Khan, Jin-Gyu Cheong, Reshma Ramaiah, Mythili Ketavarapu, Eva Kaufmann, Michael S. Glickman, Ajitha Thanabalasuriar, Steven Z. Josefowicz, Maziar Divangahi
{"title":"A fungal-derived adjuvant amplifies the antitumoral potency of Bacillus Calmette-Guérin via reprogramming granulopoiesis","authors":"Leonardo F. Jurado, Andrew W. Daman, Ziyi Li, Vanessa M.S. Ross, Kristina Nikolaou, Kim A. Tran, Oleg Loutochin, Victor A. McPherson, Renaud Prével, Raquel Tarancón, Katalina Couto, Erwan Pernet, Nargis Khan, Jin-Gyu Cheong, Reshma Ramaiah, Mythili Ketavarapu, Eva Kaufmann, Michael S. Glickman, Ajitha Thanabalasuriar, Steven Z. Josefowicz, Maziar Divangahi","doi":"10.1016/j.immuni.2025.05.026","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.05.026","url":null,"abstract":"In patients with non-muscle invasive bladder cancer, the standard immunotherapy involves intravesical Bacillus Calmette-Guérin (BCG). However, its success requires repeated doses, and ∼50% of patients do not benefit. Using a preclinical orthotopic bladder cancer model, we found that a single intravesical dose of combined BCG and β-glucan immunotherapy eradicated aggressive tumors, resulting in 100% survival. Through single-cell transcriptomic/epigenomic analysis, flow cytometry, and intravital imaging, we show that BCG and β-glucan reprogrammed hematopoietic stem and progenitor cells with imprinting in innate immune cells, particularly neutrophils. Reprogrammed neutrophils exhibited increased reactive oxygen species (ROS) production and infiltration into the tumor core, reducing tumor vascularization and growth. The tumor microenvironment can convert neutrophils into protumor cells; BCG and β-glucan prevented this conversion, promoting sustained antitumoral activity. These findings support β-glucan as a safe, effective adjuvant to enhance BCG immunotherapy in bladder cancer and other solid tumors.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"45 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144341295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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