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Differentiation of tissue-resident NK cells: Why origin and context matter 组织常驻NK细胞的分化:为什么起源和环境问题
IF 32.4 1区 医学
Immunity Pub Date : 2025-03-11 DOI: 10.1016/j.immuni.2025.02.020
Christin Friedrich, Tommaso Torcellan, Georg Gasteiger
{"title":"Differentiation of tissue-resident NK cells: Why origin and context matter","authors":"Christin Friedrich, Tommaso Torcellan, Georg Gasteiger","doi":"10.1016/j.immuni.2025.02.020","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.020","url":null,"abstract":"<h2>Section snippets</h2><section><section><h2>Main text</h2>In their letter to <em>Immunity</em>, Degli-Esposti and colleagues<sup>1</sup> discuss the potential origins of tissue-resident natural killer (trNK) cells and the inflammatory contexts enabling their differentiation. These largely unresolved issues are relevant for NK-based cellular therapies and our understanding of tissue immunity. Here, we examine key complementarities and differences between their work and our recent work,<sup>2</sup> highlighting future challenges and open research questions.TrNK cells are found in a</section></section><section><section><h2>Declaration of interests</h2>The authors declare no competing interests.</section></section>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"10 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589991","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}
引用次数: 0
The CREscendoing promise of HDAC targeting to limit atherosclerosis HDAC靶向限制动脉粥样硬化的前景
IF 32.4 1区 医学
Immunity Pub Date : 2025-03-11 DOI: 10.1016/j.immuni.2025.02.010
Máté G. Kiss, Christoph J. Binder
{"title":"The CREscendoing promise of HDAC targeting to limit atherosclerosis","authors":"Máté G. Kiss, Christoph J. Binder","doi":"10.1016/j.immuni.2025.02.010","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.010","url":null,"abstract":"The factors that modulate the inflammatory response in atherosclerosis are not well defined. In this issue of <em>Immunity</em>, Asare et al. examine the impact of a <em>cis</em>-regulatory element (CRE) that controls expression of <em>HDAC9</em> and find that HDAC9-mediated deacetylation of NLRP3 might be the mechanism by which genetic variants in this conserved CRE influence the inflammation associated with human atherosclerosis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"29 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589988","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}
引用次数: 0
Immo-bile-izing CD8+ T cell anti-tumor immunity 固定化CD8+ T细胞抗肿瘤免疫
IF 32.4 1区 医学
Immunity Pub Date : 2025-03-11 DOI: 10.1016/j.immuni.2025.02.015
Scott A. Read, Golo Ahlenstiel
{"title":"Immo-bile-izing CD8+ T cell anti-tumor immunity","authors":"Scott A. Read, Golo Ahlenstiel","doi":"10.1016/j.immuni.2025.02.015","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.015","url":null,"abstract":"Hepatocellular carcinoma is poorly responsive to immune checkpoint blockade. In a recent issue of <em>Science</em>, Varanasi et al. reveal how bile acids dampen anti-tumor CD8<sup>+</sup> T cell responses in the liver, contributing to cancer progression and poor immunotherapy outcomes.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"29 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143590051","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}
引用次数: 0
RIPK3: The Deadpool of neuronal cell death proteins? RIPK3:神经元细胞死亡蛋白的死池?
IF 32.4 1区 医学
Immunity Pub Date : 2025-03-11 DOI: 10.1016/j.immuni.2025.02.018
Clayton W. Winkler, Karin E. Peterson
{"title":"RIPK3: The Deadpool of neuronal cell death proteins?","authors":"Clayton W. Winkler, Karin E. Peterson","doi":"10.1016/j.immuni.2025.02.018","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.018","url":null,"abstract":"Receptor interaction kinase 3 (RIPK3) is a key mediator of necroptosis, initiating programmed cell death with mercenary efficiency in multiple neurodegenerative diseases. However, in this issue of <em>Immunity</em>, Estevez et al. demonstrate that RIPK3, like the character Deadpool, exists in duality and can also be a force for good by preventing excitotoxic neuronal death during orthoflavivirus encephalitis.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"31 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143590053","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}
引用次数: 0
Antigenic drift expands influenza viral escape pathways from recalled humoral immunity 抗原漂移扩大了流感病毒从体液免疫中逃逸的途径
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.006
Daniel P. Maurer, Mya Vu, Aaron G. Schmidt
{"title":"Antigenic drift expands influenza viral escape pathways from recalled humoral immunity","authors":"Daniel P. Maurer, Mya Vu, Aaron G. Schmidt","doi":"10.1016/j.immuni.2025.02.006","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.006","url":null,"abstract":"Initial exposure to a rapidly evolving virus establishes B cell memory that biases later responses to antigenically drifted strains. This “immune imprinting” implies that subsequent exposure to a drifted strain can induce affinity maturation of memory B cells toward cross-reactivity with the drifted strain and hence toward greater overall breadth. Here, we used deep mutational scanning of H1 influenza hemagglutinins (HAs) to investigate how viruses evolve in response to these broad antibody response. We identified escape mutations from clonal antibody lineages that targeted the receptor binding site and lateral patch. By adjusting the antigen-antibody contacts, antibody affinity maturation restricted the potential escape routes for the eliciting strain. However, escape occurred readily in drifted strains. We attribute this escape-prone property of the drifted strains to epistatic networks within HA. Our data explain how the influenza virus continues to evolve in the human population by escaping even broad antibody responses.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"23 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518151","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}
引用次数: 0
A heart-brain-spleen axis controls cardiac remodeling to hypertensive stress 心脏-脑-脾轴控制高血压应激下的心脏重塑
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.013
Sara Perrotta, Lorenzo Carnevale, Marialuisa Perrotta, Fabio Pallante, Tomasz P. Mikołajczyk, Valentina Fardella, Agnese Migliaccio, Stefania Fardella, Sara Nejat, Boguslaw Kapelak, Azzurra Zonfrilli, Jacopo Pacella, Francesco Mastroiacovo, Raimondo Carnevale, Calum Bain, Sarah Lena Puhl, Giuseppe D’Agostino, Slava Epelman, Tomasz J. Guzik, Giuseppe Lembo, Daniela Carnevale
{"title":"A heart-brain-spleen axis controls cardiac remodeling to hypertensive stress","authors":"Sara Perrotta, Lorenzo Carnevale, Marialuisa Perrotta, Fabio Pallante, Tomasz P. Mikołajczyk, Valentina Fardella, Agnese Migliaccio, Stefania Fardella, Sara Nejat, Boguslaw Kapelak, Azzurra Zonfrilli, Jacopo Pacella, Francesco Mastroiacovo, Raimondo Carnevale, Calum Bain, Sarah Lena Puhl, Giuseppe D’Agostino, Slava Epelman, Tomasz J. Guzik, Giuseppe Lembo, Daniela Carnevale","doi":"10.1016/j.immuni.2025.02.013","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.013","url":null,"abstract":"Hypertensive heart disease (HTN-HD) meaningfully contributes to hypertension morbidity and mortality. Initially established as an adaptive response, HTN-HD progresses toward worsening of left ventricule (LV) function and heart failure (HF). Hypertensive stress elevates sympathetic nervous system (SNS) activity, a negative clinical predictor, and expands macrophages. How they interact in the compensatory phase of HTN-HD is unclear. We report that LV pressure overload recruited a brainstem neural circuit to enhance splenic SNS and induce placental growth factor (PlGF) secretion. During hypertensive stress, PlGF drove the proliferation of self-renewing cardiac resident macrophages (RMs) expressing its receptor neuropilin-1 (NRP1). Inhibition of the splenic neuroimmune axis or ablation of NRP1 in RM hindered the adaptive response to hypertensive stress, leading to HF. In humans, circulating PlGF correlated with cardiac hypertrophy, and failing hearts expressed NRP1 in RMs. Here, we discovered a multiorgan response driving a neural reflex to expand cardiac NRP1+ RM and counteract HF.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"15 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518153","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}
引用次数: 0
IL-17RA signaling provides dual tumor-suppressor function during late-stage colorectal carcinogenesis IL-17RA信号在晚期结直肠癌发生过程中提供双重肿瘤抑制功能
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.005
Dominic Denk, Mallika Ramakrishnan, Claire Conche, Charles Pallangyo, Marina Pesic, Fatih Ceteci, Kilian B. Kennel, Asude C. Kirisözü, Esther Engel, Kathleen Mohs, Birgit Ritter, Angeles Macias Pardo, Ezgi Özkurt, Falk Hildebrand, Ari Waisman, Melek C. Arkan, Florian R. Greten
{"title":"IL-17RA signaling provides dual tumor-suppressor function during late-stage colorectal carcinogenesis","authors":"Dominic Denk, Mallika Ramakrishnan, Claire Conche, Charles Pallangyo, Marina Pesic, Fatih Ceteci, Kilian B. Kennel, Asude C. Kirisözü, Esther Engel, Kathleen Mohs, Birgit Ritter, Angeles Macias Pardo, Ezgi Özkurt, Falk Hildebrand, Ari Waisman, Melek C. Arkan, Florian R. Greten","doi":"10.1016/j.immuni.2025.02.005","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.005","url":null,"abstract":"Expression of interleukin (IL)-17 family cytokines is associated with tumor-promoting inflammation. We found that low expression of <em>IL17RA</em> associated with worse prognosis in late-stage colorectal cancer (CRC) patients. Deletion of <em>Il17ra</em> in intestinal epithelial cells (IECs) in a murine model of CRC enhanced epithelial-to-mesenchymal transition (EMT) via increased expression of the epidermal growth factor receptor and subsequent activation of the kinase Src. Yet, these mice were protected from metastatic disease; <em>Il17ra</em> deletion impaired intestinal barrier function and enhanced systemic fungal invasion and associated immunity. However, in macrophages, IL-17RA was required for spleen tyrosine kinase (Syk) activation upon fungal-induced dectin-1 engagement, and <em>Il17ra</em> ablation impaired IL-18 release and protective CD8<sup>+</sup> T cell-mediated anti-tumor immunity. Combining recombinant IL-17 and heat-killed <em>Candida albicans</em> rendered colorectal tumors sensitive to α-PD-1 treatment in a model of microsatellite stable (MSS) CRC. Thus, IL-17RA engages two distinct tumor-suppressive mechanisms in CRC, linking EMT and fungal-induced anti-tumor immunity during tumor progression.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"51 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518154","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}
引用次数: 0
Collaboration between interleukin-7 and -15 enables adaptation of tissue-resident and circulating memory CD8+ T cells to cytokine deficiency 白细胞介素-7和-15之间的协作使组织驻留和循环记忆CD8+ T细胞适应细胞因子缺乏
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.009
Nicholas N. Jarjour, Talia S. Dalzell, Nicholas J. Maurice, Kelsey M. Wanhainen, Changwei Peng, Stephen D. O’Flanagan, Taylor A. DePauw, Katharine E. Block, William J. Valente, K. Maude Ashby, David Masopust, Stephen C. Jameson
{"title":"Collaboration between interleukin-7 and -15 enables adaptation of tissue-resident and circulating memory CD8+ T cells to cytokine deficiency","authors":"Nicholas N. Jarjour, Talia S. Dalzell, Nicholas J. Maurice, Kelsey M. Wanhainen, Changwei Peng, Stephen D. O’Flanagan, Taylor A. DePauw, Katharine E. Block, William J. Valente, K. Maude Ashby, David Masopust, Stephen C. Jameson","doi":"10.1016/j.immuni.2025.02.009","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.009","url":null,"abstract":"Interleukin-7 (IL-7) is considered a critical regulator of memory CD8<sup>+</sup> T cell homeostasis. However, this is primarily based on circulating memory populations, and the cell-intrinsic requirement for IL-7 signaling during memory homeostasis has not been directly tested. Here, we addressed the role for IL-7Rα in circulating and resident memory CD8<sup>+</sup> T cells (Trm) after their establishment. We found that inducible <em>Il7ra</em> deletion had only a modest effect on persistence of circulating memory and Trm subsets, causing reduced basal proliferation. Loss of IL-15 signaling imposed heightened IL-7Rα dependence on memory CD8<sup>+</sup> T cells, including Trm cells described as IL-15 independent. In the absence of IL-15 signaling, IL-7Rα was elevated, and loss of IL-7Rα signaling reduced IL-15-elicited proliferation, suggesting crosstalk between these pathways in memory CD8<sup>+</sup> T cells. Thus, across subsets and tissues, IL-7 and IL-15 act in concert to support memory CD8<sup>+</sup> T cells, conferring resilience to altered availability of either cytokine.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"40 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518547","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}
引用次数: 0
Splenic TNF-α signaling potentiates the innate-to-adaptive transition of antiviral NK cells 脾TNF-α信号增强了抗病毒NK细胞的先天向适应性转变
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.012
Adriana M. Mujal, Mark Owyong, Endi K. Santosa, John C. Sauter, Simon Grassmann, Anna-Marie Pedde, Philippa Meiser, Claire K. Wingert, Marine Pujol, Veit R. Buchholz, Colleen M. Lau, Jan P. Böttcher, Joseph C. Sun
{"title":"Splenic TNF-α signaling potentiates the innate-to-adaptive transition of antiviral NK cells","authors":"Adriana M. Mujal, Mark Owyong, Endi K. Santosa, John C. Sauter, Simon Grassmann, Anna-Marie Pedde, Philippa Meiser, Claire K. Wingert, Marine Pujol, Veit R. Buchholz, Colleen M. Lau, Jan P. Böttcher, Joseph C. Sun","doi":"10.1016/j.immuni.2025.02.012","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.012","url":null,"abstract":"Natural killer (NK) cells possess both innate and adaptive features. Here, we investigated NK cell activation across tissues during cytomegalovirus infection, which generates antigen-specific clonal expansion and long-lived memory responses. Longitudinal tracking and single-cell RNA sequencing of NK cells following infection revealed enhanced activation in the spleen, as well as early formation of a CD69<sup>lo</sup> precursor population that preferentially gave rise to adaptive NK cells. Splenic NK cells demonstrated heightened tumor necrosis factor alpha (TNF-α) signaling and increased expression of the receptor TNFR2, which coincided with elevated TNF-α production by splenic myeloid cells. TNFR2-deficient NK cells exhibited impaired interferon gamma (IFN-γ) production and expansion. TNFR2 signaling engaged two distinct nuclear factor κB (NF-κB) signaling arms—innate effector NK cell responses required canonical NF-κB signaling, whereas non-canonical NF-κB signaling enforced differentiation of CD69<sup>lo</sup> adaptive NK cell precursors. Thus, NK cell priming in the spleen during viral infection promotes an innate-to-adaptive transition, providing insight into avenues for generating adaptive NK cell immunity across diverse settings.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"28 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518149","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}
引用次数: 0
Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis 胆汁酸受体FXR促进新生儿坏死性小肠结肠炎的肠上皮铁上落和随后的ILC3功能障碍
IF 32.4 1区 医学
Immunity Pub Date : 2025-02-28 DOI: 10.1016/j.immuni.2025.02.003
Yuxin Zhang, Yuchao Jing, Juan He, Rui Dong, Tongyang Li, Fang Li, Xiaoqing Zheng, Gaoyu Liu, Ran Jia, Jin Xu, Fan Wu, Chunhong Jia, Jin Song, Lijuan Zhang, Pan Zhou, Haitao Wang, Zhi Yao, Qiang Liu, Ying Yu, Jie Zhou
{"title":"Bile acid receptor FXR promotes intestinal epithelial ferroptosis and subsequent ILC3 dysfunction in neonatal necrotizing enterocolitis","authors":"Yuxin Zhang, Yuchao Jing, Juan He, Rui Dong, Tongyang Li, Fang Li, Xiaoqing Zheng, Gaoyu Liu, Ran Jia, Jin Xu, Fan Wu, Chunhong Jia, Jin Song, Lijuan Zhang, Pan Zhou, Haitao Wang, Zhi Yao, Qiang Liu, Ying Yu, Jie Zhou","doi":"10.1016/j.immuni.2025.02.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2025.02.003","url":null,"abstract":"Necrotizing enterocolitis (NEC) is a common pediatric emergency primarily afflicting preterm infants, yet its mechanisms remain to be fully understood. Here, we report that plasma fibroblast growth factor (FGF)19, a target of farnesoid X receptor (FXR), was positively correlated with the clinical parameters of NEC. NEC patients and the NEC murine model displayed abundant FXR in intestinal epithelial cells (IECs), which was restricted by microbiota-derived short-chain fatty acids (SCFAs) under homeostasis. Genetic deficiency of FXR in IECs caused remission of NEC. Mechanistically, FXR facilitated ferroptosis of IECs via targeting acyl-coenzyme A synthetase long-chain family member 4 (<em>Acsl4</em>). Lipid peroxides released by ferroptotic IECs suppressed interleukin (IL)-22 secretion from type 3 innate lymphoid cells (ILC3s), thereby exacerbating NEC. Intestinal FXR antagonist, ACSL4 inhibitor, and ferroptosis inhibitor ameliorated murine NEC. Furthermore, the elevated lipid peroxides in NEC patients were positively correlated with FGF19 and disease parameters. These observations demonstrate the therapeutic value of targeting intestinal FXR and ferroptosis in NEC treatment.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"66 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518150","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}
引用次数: 0
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