Cellular &Molecular Immunology最新文献_第4页

Liver macrophages: development, dynamics, and functions. 肝巨噬细胞：发育、动态和功能。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-03 DOI: 10.1038/s41423-025-01298-3

Ysbrand Nusse, Paul Kubes

{"title":"Liver macrophages: development, dynamics, and functions.","authors":"Ysbrand Nusse, Paul Kubes","doi":"10.1038/s41423-025-01298-3","DOIUrl":"https://doi.org/10.1038/s41423-025-01298-3","url":null,"abstract":"The liver is a sizeable visceral organ whose primary functions involve nutrient metabolism, clearance of toxins, and energy storage. Besides these critical functions, the liver is also a major immunological site. It is populated by several specialized resident immune cells, including B cells, T Cells, dendritic cells, and several populations of macrophages. It is also the site for the production and release of acute-phase proteins during inflammation. One reason for garrisoning these immune sentinels and effectors in the liver is its relative location in the circulatory system. The liver is the first significant organ downstream of the intestine, where blood originating from the intestine enters the liver through the portal vein. This organization facilitates the liver's uptake and processing of nutrient-rich blood directly from the intestinal source. However, the intestine is also home to trillions of microbes, many of which are commensals but also represent potential pathogens. As such, the portal blood supply represents an avenue for systemic infection. To sterilize the portal blood, the liver immune system filters pathogens, which is primarily accomplished by liver macrophages. Here, we will discuss the major populations of macrophages resident in the liver, their location, functions, development, and role in maintaining the liver in the face of injury and infection.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":""},"PeriodicalIF":21.8,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215091","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

Harnessing nutrient scarcity for enhanced CAR-T-cell potency and safety in solid tumors. 利用营养稀缺增强car - t细胞在实体肿瘤中的效力和安全性。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-05-08 DOI: 10.1038/s41423-025-01290-x

Enzo Manchon, Nell Hirt, Benjamin Versier, Aravindhan Soundiramourty, Ludmila Juricek, Celeste Lebbe, Maxime Battistella, Yves Christen, Jacques Mallet, Dominique Charron, Nabila Jabrane-Ferrat, Che Serguera, Reem Al-Daccak

{"title":"Harnessing nutrient scarcity for enhanced CAR-T-cell potency and safety in solid tumors.","authors":"Enzo Manchon, Nell Hirt, Benjamin Versier, Aravindhan Soundiramourty, Ludmila Juricek, Celeste Lebbe, Maxime Battistella, Yves Christen, Jacques Mallet, Dominique Charron, Nabila Jabrane-Ferrat, Che Serguera, Reem Al-Daccak","doi":"10.1038/s41423-025-01290-x","DOIUrl":"10.1038/s41423-025-01290-x","url":null,"abstract":"Despite significant advancements, the effectiveness of chimeric antigen receptor (CAR)-T-cell-based therapies in solid tumors remains limited. Key challenges include on-target effects, off-tumor toxicity and reduced CAR-T-cell function within the tumor microenvironment, which is often characterized by metabolic stress triggered by factors such as amino acid scarcity. Activating transcription factor-4 (ATF4) and its upstream regulator GCN2 play crucial roles in the metabolic reprogramming and functionality of CD4+ and CD8+ T cells. ATF4 can be activated by various cellular stress signals, including amino acid deprivation. While ATF4 activation may be associated with T-cell dysfunction, its role in stress adaptation presents an opportunity for therapeutic intervention-particularly in the tumor microenvironment, where T-cell exhaustion is a major challenge. In this study, we developed a strategy to harness the GCN2‒ATF4 axis in CAR-T cells. We employed an amino acid-dependent inducible promoter, which triggers ATF4-dependent gene expression to regulate CAR expression in T cells under conditions of amino acid scarcity within the tumor microenvironment. In vitro and murine xenograft models demonstrate the potential of this system to effectively restrict CAR expression to the tumor site. This targeted strategy not only enhances safety by minimizing off-tumor activity but also CAR-T-cell fitness by reducing exhaustion. By validating this pathophysiologically regulatable CAR expression system for solid tumors, our findings address key limitations of current CAR-T-cell therapies and pave the way for innovative strategies targeting solid malignancies.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"645-660"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143955224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Activation and maturation of antigen-specific B cells in nonectopic lung infiltrates are independent of germinal center reactions in the draining lymph node. 非异位肺浸润中抗原特异性B细胞的激活和成熟与引流淋巴结的生发中心反应无关。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-04-11 DOI: 10.1038/s41423-025-01285-8

Sarah-Sophie Schacht, Josefine Graffunder, Pawel Durek, Jonas Wehrenberg, Annette Siracusa, Charlotte Biese, Mir-Farzin Mashreghi, Kevin Thurley, Laura Bauer, Andreas Hutloff

{"title":"Activation and maturation of antigen-specific B cells in nonectopic lung infiltrates are independent of germinal center reactions in the draining lymph node.","authors":"Sarah-Sophie Schacht, Josefine Graffunder, Pawel Durek, Jonas Wehrenberg, Annette Siracusa, Charlotte Biese, Mir-Farzin Mashreghi, Kevin Thurley, Laura Bauer, Andreas Hutloff","doi":"10.1038/s41423-025-01285-8","DOIUrl":"10.1038/s41423-025-01285-8","url":null,"abstract":"Pulmonary T and B cells are important for protection of this mucosal barrier site. While viral infections lead to the development of ectopic lymphoid structures highly similar to those in germinal centers in secondary lymphoid organs, little is known about how T/B cooperation occurs in the unstructured, diffuse tissue infiltrates characteristic of autoimmune diseases and nonviral infections. Using a mouse model of interstitial lung inflammation, we found that naive B cells are directly activated in lung tissue. Despite the absence of any germinal center-like structures, the interaction of B cells with peripheral T helper cells results in efficient somatic hypermutation and class switching. As antigen-presenting cells, macrophages are critical for this process. Unique B-cell repertoires indicated that the lung response was autonomous from the lung-draining lymph node. Only lung GC-like B cells were switched to IgA and had a broader repertoire, making them ideal candidates for producing broadly neutralizing immunoglobulins against respiratory pathogens.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"612-627"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

FXR protects against neonatal sepsis by enhancing the immunosuppressive function of MDSCs. FXR通过增强MDSCs的免疫抑制功能来预防新生儿脓毒症。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-05-08 DOI: 10.1038/s41423-025-01289-4

Juan He, Yuxin Zhang, Yuchao Jing, Rui Dong, Tongyang Li, Xiaoqing Zheng, Pan Zhou, Kun Shi, Wei Zhong, Qiang Liu, Jie Zhou

{"title":"FXR protects against neonatal sepsis by enhancing the immunosuppressive function of MDSCs.","authors":"Juan He, Yuxin Zhang, Yuchao Jing, Rui Dong, Tongyang Li, Xiaoqing Zheng, Pan Zhou, Kun Shi, Wei Zhong, Qiang Liu, Jie Zhou","doi":"10.1038/s41423-025-01289-4","DOIUrl":"10.1038/s41423-025-01289-4","url":null,"abstract":"Myeloid-derived suppressor cells (MDSCs) play a protective role against neonatal inflammation during the early postnatal period. However, the mechanisms regulating neonatal MDSC function remain to be fully elucidated. In this study, we report that the bile acid receptor farnesoid X receptor (FXR) acts as a positive regulator of neonatal MDSC function. The FDA-approved FXR agonist obeticholic acid (OCA) protects against neonatal sepsis in an FXR-dependent manner. Genetic deficiency of FXR impairs the immunosuppressive and antibacterial functions of MDSCs, thereby exacerbating the severity of neonatal sepsis. Adoptive transfer of MDSCs alleviates sepsis in both Fxr-/- and Fxrfl/flMrp8-Cre+ pups. Mechanistic studies revealed that Hif1α, a well-established regulator of MDSCs, is a direct transcriptional target of FXR. In patients with neonatal sepsis, downregulation of FXR and HIF-1α in MDSCs was observed, which was inversely correlated with clinical parameters. These observations demonstrate the importance of FXR in neonatal MDSC function and its therapeutic potential in neonatal sepsis.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"661-673"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Updated insights into the molecular networks for NLRP3 inflammasome activation. NLRP3炎性小体激活分子网络的最新见解。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-04-30 DOI: 10.1038/s41423-025-01284-9

Seungwha Paik, Jin Kyung Kim, Hyo Jung Shin, Eun-Jin Park, In Soo Kim, Eun-Kyeong Jo

{"title":"Updated insights into the molecular networks for NLRP3 inflammasome activation.","authors":"Seungwha Paik, Jin Kyung Kim, Hyo Jung Shin, Eun-Jin Park, In Soo Kim, Eun-Kyeong Jo","doi":"10.1038/s41423-025-01284-9","DOIUrl":"10.1038/s41423-025-01284-9","url":null,"abstract":"Over the past decade, significant advances have been made in our understanding of how NACHT-, leucine-rich-repeat-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes are activated. These findings provide detailed insights into the transcriptional and posttranslational regulatory processes, the structural-functional relationship of the activation processes, and the spatiotemporal dynamics of NLRP3 activation. Notably, the multifaceted mechanisms underlying the licensing of NLRP3 inflammasome activation constitute a focal point of intense research. Extensive research has revealed the interactions of NLRP3 and its inflammasome components with partner molecules in terms of positive and negative regulation. In this Review, we provide the current understanding of the complex molecular networks that play pivotal roles in regulating NLRP3 inflammasome priming, licensing and assembly. In addition, we highlight the intricate and interconnected mechanisms involved in the activation of the NLRP3 inflammasome and the associated regulatory pathways. Furthermore, we discuss recent advances in the development of therapeutic strategies targeting the NLRP3 inflammasome to identify potential therapeutics for NLRP3-associated inflammatory diseases. As research continues to uncover the intricacies of the molecular networks governing NLRP3 activation, novel approaches for therapeutic interventions against NLRP3-related pathologies are emerging.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"563-596"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

The NET-DNA-CCDC25 inhibitor di-Pal-MTO suppresses tumor progression and promotes the innate immune response. NET-DNA-CCDC25抑制剂di-Pal-MTO抑制肿瘤进展并促进先天免疫反应。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-04-14 DOI: 10.1038/s41423-025-01286-7

Shun Wang, Xinyan Liang, Heliang Li, Junying Zou, Linxi Xu, Yetong Zhang, Jianghua Lin, Jiayi Zeng, Xiaoming Zhong, Xu Liu, Zhou Liu, Yue Zheng, Man Nie, Linbin Yang

{"title":"The NET-DNA-CCDC25 inhibitor di-Pal-MTO suppresses tumor progression and promotes the innate immune response.","authors":"Shun Wang, Xinyan Liang, Heliang Li, Junying Zou, Linxi Xu, Yetong Zhang, Jianghua Lin, Jiayi Zeng, Xiaoming Zhong, Xu Liu, Zhou Liu, Yue Zheng, Man Nie, Linbin Yang","doi":"10.1038/s41423-025-01286-7","DOIUrl":"10.1038/s41423-025-01286-7","url":null,"abstract":"The DNA component of neutrophil extracellular traps (NET-DNA) is associated with cancer metastasis and chemotherapy resistance. However, recent studies have suggested that NET-DNA contributes to the activation of dendritic cells (DCs) and promotes the innate immune response to anticancer immunity. Therefore, exploring therapeutic approaches to inhibit NET-mediated tumor progression while maintaining antitumor immunity is essential. Our groups recently identified CCDC25 as a specific NET-DNA sensor on the cytoplasmic membrane of cancer cells that promotes cancer metastasis. In this study, we performed small-molecule compound screening and revealed that mitoxantrone (MTO) could block the interaction between NET-DNA and CCDC25. Molecular docking results indicated that MTO competed with NET-DNA by binding with the amino acid residues Tyr24 (Y24), Glu25 (E25), and Asp28 (D28) of the crystal structure of CCDC25. More importantly, we conjugated MTO with palmitoleic acids such as di-Pal-MTO to increase its residence time on the cytoplasmic membrane, which increased its inhibitory efficiency and decreased its cytotoxicity. In addition, di-Pal-MTO markedly inhibited the RAC1-CDC42 cascade to alleviate the NET-induced cytoskeleton arrangement and chemotactic migration of cancer cells. In multiple mouse models, di-Pal-MTO can suppress breast cancer metastasis and have synergistic effects with chemotherapeutics. Moreover, di-Pal-MTO promotes NET-DNA-dependent DC activation, leading to the subsequent expression of various chemokines that facilitate the infiltration of CD8+ T cells. Overall, we successfully identified a small molecule inhibitor, di-Pal-MTO, with dual effects on tumor repression and the antitumor immune response, which provides a novel therapeutic strategy against breast cancer.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"628-644"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Malonate promotes CD8⁺ T cell memory formation via protein malonylation. 丙二酸盐通过蛋白丙二酸化促进CD8+ T细胞记忆形成。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-05-14 DOI: 10.1038/s41423-025-01294-7

Qianqian Duan, Jiajia Wang, Liang Sun, Zihan Chen, Wenhui Li, Xiaowei Liu, Aijun Zhang, Yong Liu, Lianjun Zhang

{"title":"Malonate promotes CD8+ T cell memory formation via protein malonylation.","authors":"Qianqian Duan, Jiajia Wang, Liang Sun, Zihan Chen, Wenhui Li, Xiaowei Liu, Aijun Zhang, Yong Liu, Lianjun Zhang","doi":"10.1038/s41423-025-01294-7","DOIUrl":"10.1038/s41423-025-01294-7","url":null,"abstract":"Protein malonylation represents a recently identified posttranslational modification whose role in CD8+ T cell differentiation and functionality remains incompletely understood. In this study, we demonstrate that enhancing protein malonylation through sodium malonate (SM) treatment promotes CD8+ T cell memory formation in response to bacterial infection, subsequently potentiating recall responses. Comparative metabolomic analysis between SM-treated and control CD8+ T cells revealed significant metabolic alterations associated with protein malonylation. We present the first comprehensive proteomic analysis of lysine malonylation in murine CD8+ T cells, identifying 77 malonylation sites across 64 proteins involved in diverse cellular processes, particularly metabolic pathways. Malonylation of STAT6 was confirmed via the use of a specific chemical probe. Notably, we established that malonylation at the lysine 374 site of STAT6 results in increased TCF1 expression, due to alleviated transcriptional repression of TCF1 by STAT6. Collectively, our findings provide compelling evidence that protein malonylation plays a significant role in regulating CD8+ T cell memory formation.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"674-689"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144076320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Author Correction: Cancer-associated fibroblasts express CD1d and activate invariant natural killer T cells under cellular stress. 作者更正：癌症相关成纤维细胞表达CD1d并在细胞应激下激活不变的自然杀伤T细胞。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 DOI: 10.1038/s41423-025-01274-x

Shengduo Pei, Jonas Sjölund, Yueyun Pan, Kristian Pietras, Mikael C I Karlsson

引用次数: 0

NETosis exacerbates skin inflammation in obese psoriasis patients. NETosis加重肥胖牛皮癣患者的皮肤炎症。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-05-20 DOI: 10.1038/s41423-025-01287-6

Bruno Marcel Silva de Melo, José Carlos Alves-Filho, Bernhard Ryffel

引用次数: 0

Saturated fatty acid-induced neutrophil extracellular traps contribute to exacerbation and biologic therapy resistance in obesity-related psoriasis. 饱和脂肪酸诱导的中性粒细胞胞外陷阱有助于肥胖相关银屑病的恶化和生物治疗抵抗。

IF 21.8 1区医学

Cellular &Molecular Immunology Pub Date : 2025-06-01 Epub Date: 2025-04-01 DOI: 10.1038/s41423-025-01278-7

Yuting Xia, Jiajia Lan, Jing Yang, Shijie Yuan, Xiaorong Xie, Qiuyang Du, Hongyao Du, Wenjia Nie, Biling Jiang, Liang Zhao, Zhen Cai, Xin Zhang, Yan Xiong, Yan Li, Ran He, Juan Tao

{"title":"Saturated fatty acid-induced neutrophil extracellular traps contribute to exacerbation and biologic therapy resistance in obesity-related psoriasis.","authors":"Yuting Xia, Jiajia Lan, Jing Yang, Shijie Yuan, Xiaorong Xie, Qiuyang Du, Hongyao Du, Wenjia Nie, Biling Jiang, Liang Zhao, Zhen Cai, Xin Zhang, Yan Xiong, Yan Li, Ran He, Juan Tao","doi":"10.1038/s41423-025-01278-7","DOIUrl":"10.1038/s41423-025-01278-7","url":null,"abstract":"Psoriasis patients who are obese tend to have serious clinical manifestations and poor responses to various biological agents in most cases. However, the mechanisms by which obesity exacerbates psoriasis remain enigmatic. In this study, we found that the abundance of systemic and localized cutaneous neutrophil extracellular traps (NETs) associated with the obesity-induced aggravation of psoriasis was positively correlated with disease severity and that the inhibition of NETs alleviated psoriatic dermatitis in obese mice. Mechanistically, we found that changes in fatty acid composition in obese subjects resulted in the deposition of saturated fatty acids (SFAs), which promoted the release of NETs via the TLR4-MD2/ROS signaling pathway. We further revealed that NETs potentiate IL-17 inflammation, especially γδT17-mediated immune responses, in obesity-exacerbated psoriasis patients. Moreover, SFAs induced a decreased response to anti-IL17A treatment in psoriasis-like mice, whereas the inhibition of NETs improved the beneficial effects of anti-IL17A in psoriasis-like mice with lipid metabolism disorders. Our findings collectively suggest that SFA-induced NETs play a critical role in the exacerbation of obesity-related psoriasis and provide potential new strategies for the clinical treatment of refractory psoriasis patients with lipid metabolism disorders.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":" ","pages":"597-611"},"PeriodicalIF":21.8,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143762518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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