Science Immunology最新文献_第5页

The 10 commandments of immunoregulation in lymphoma 淋巴瘤免疫调节的十诫

IF 17.6 1区医学

Science Immunology Pub Date : 2025-07-04 DOI: 10.1126/sciimmunol.aea0950

Maria de los Reyes Capilla Guerra, Gabriel K. Griffin

引用次数: 0

Tuft cells restrain intestinal type 2 immunity through the transcription factor Spi-B 簇毛细胞通过转录因子Spi-B抑制肠道2型免疫

IF 17.6 1区医学

Science Immunology Pub Date : 2025-07-04 DOI: 10.1126/sciimmunol.ads5818

Jiali Wang, Ruoxi Shen, Kunpeng Yang, Xiaohuan Guo, Jingyou Yu, Chuan Wu, Xue-Kun Guo, Xiaoyu Hu

{"title":"Tuft cells restrain intestinal type 2 immunity through the transcription factor Spi-B","authors":"Jiali Wang, Ruoxi Shen, Kunpeng Yang, Xiaohuan Guo, Jingyou Yu, Chuan Wu, Xue-Kun Guo, Xiaoyu Hu","doi":"10.1126/sciimmunol.ads5818","DOIUrl":"10.1126/sciimmunol.ads5818","url":null,"abstract":"<div >Excessive type 2 immunity underlies various disease conditions, including allergies, yet the homeostatic mechanisms that limit type 2 responses are not fully understood. Here, we revealed that intestinal tuft cells, specialized epithelial cells known for triggering type 2 immune activation, also have a molecular circuit that restrains type 2 responses. Ablation of the transcription factor Spi-B in tuft cells was sufficient to elicit spontaneous type 2 inflammation. Tuft cell–intrinsic deficiency of Spi-B rendered otherwise resistant C57BL/6J mice susceptible to food allergy models. Spi-B repressed c-Kit signaling–driven production of the type 2 alarmin TSLP by tuft cells. Disruption of this negative regulatory axis led to tuft cell hyperplasia and exacerbated type 2 inflammation, which could be pharmacologically targeted with a tyrosine kinase inhibitor. These findings pinpoint a crucial tuft cell–centric checkpoint of type 2 immunity and highlight the dual role of tuft cells in both promoting and restraining type 2 responses.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 109","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads5818","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144558273","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

TB or not TB: That depends on the antibody Fc 结核病或非结核病：这取决于抗体Fc

IF 17.6 1区医学

Science Immunology Pub Date : 2025-07-04 DOI: 10.1126/sciimmunol.aea0953

Surabhi Kumar, Kevin C. O’Connor

引用次数: 0

Primate retroelement exonization and sexually dimorphic IL13RA1 transcription tune type 2 immune responses 灵长类逆转录因子外显子和两性二态IL13RA1转录调节2型免疫应答

IF 17.6 1区医学

Science Immunology Pub Date : 2025-07-04 DOI: 10.1126/sciimmunol.adr1105

Tobias Plowman, Tom Hofland, Callum Hall, Rachael Thompson, Judith Pape, Kevin W. Ng, Laura Doglio, George Kassiotis

{"title":"Primate retroelement exonization and sexually dimorphic IL13RA1 transcription tune type 2 immune responses","authors":"Tobias Plowman, Tom Hofland, Callum Hall, Rachael Thompson, Judith Pape, Kevin W. Ng, Laura Doglio, George Kassiotis","doi":"10.1126/sciimmunol.adr1105","DOIUrl":"10.1126/sciimmunol.adr1105","url":null,"abstract":"<div >Type 2 immunity is orchestrated by IL-4 and IL-13 signaling, initiated by binding to receptors that are specific to each cytokine or to the shared heterodimeric receptor comprising the IL-4Rα and IL-13Rα1 subunits. Here, we report that sexually dimorphic <i>IL13RA1</i> transcription is regulated by estrogen and characterize an IL-13Rα1 isoform (referred to here as IL-13Rα1–LOR1a) created through facultative splicing to an alternative terminal exon composed of primate-specific retrotransposable elements (RTEs). At the mRNA level, RTE exonization replaces regulatory sequences in the canonical 3′ untranslated region (3′UTR) implicated in <i>IL13RA1</i> mRNA stability. Moreover, alternative splicing removes critical domains in the cytoplasmic tail, rendering the IL-13Rα1–LOR1a isoform partially signaling defective at the protein level. When coexpressed, the IL-13Rα1–LOR1a isoform antagonizes the function of the canonical receptor, reducing cellular responsiveness to IL-4 and IL-13. Thus, the balance of the two <i>IL13RA1</i> isoforms appears to fine-tune type 2 cytokine signaling and downstream immune responses.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 109","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144558271","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

Riplet promotes lipid metabolism changes associated with CD8 T cell exhaustion and anti–PD-1 resistance in hepatocellular carcinoma Riplet促进肝细胞癌中与CD8 T细胞衰竭和抗pd -1耐药相关的脂质代谢变化

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-27 DOI: 10.1126/sciimmunol.ado3485

Junnan Liang, Jingyu Liao, Ruizhi Chang, Wenlong Jia, Ganxun Li, Zeyu Chen, Hang Wu, Chang Zhu, Jingyuan Wen, Qibo Huang, Han Gao, Zichen Gui, Weiqi Xu, Huifang Liang, Qiumeng Liu, Dafeng Xu, Zifu Li, Limin Xia, Xiaoping Chen, Zhao Huang, Wanguang Zhang, Zeyang Ding, Bixiang Zhang

{"title":"Riplet promotes lipid metabolism changes associated with CD8 T cell exhaustion and anti–PD-1 resistance in hepatocellular carcinoma","authors":"Junnan Liang, Jingyu Liao, Ruizhi Chang, Wenlong Jia, Ganxun Li, Zeyu Chen, Hang Wu, Chang Zhu, Jingyuan Wen, Qibo Huang, Han Gao, Zichen Gui, Weiqi Xu, Huifang Liang, Qiumeng Liu, Dafeng Xu, Zifu Li, Limin Xia, Xiaoping Chen, Zhao Huang, Wanguang Zhang, Zeyang Ding, Bixiang Zhang","doi":"10.1126/sciimmunol.ado3485","DOIUrl":"10.1126/sciimmunol.ado3485","url":null,"abstract":"<div >The overall response rate to immunotherapy is modest in hepatocellular carcinoma (HCC), and immunotherapy resistance mechanisms are incompletely understood. We report that the E3 ubiquitin ligase <i>Riplet</i> is universally silenced by promoter hypermethylation in HCC. Loss of <i>Riplet</i> modulates fatty acid metabolism to promote terminal exhaustion of CD8 T cells. Riplet loss impedes K48-linked polyubiquitination of fatty acid synthase (FASN), consequently accelerating fatty acid production in HCC. Tumor cell–derived free fatty acids, especially palmitic acid (PA/C16:0), activate STAT3 (signal transducers and activators of transcription 3) by enhancing its palmitoylation in T cells, consequently triggering terminal CD8 T cell exhaustion. HCC cells with Riplet deficiency are resistant to anti–PD-1 therapy, and treatment with an FASN inhibitor overcomes resistance. Our study shows how Riplet can alter lipid metabolism and induce CD8 T cell exhaustion and anti–PD-1 resistance, thus suggesting avenues for combined therapies for treating patients with Riplet-deficient HCC.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144500476","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

Radiotherapy enhances anticancer CD8 T cell responses by cGAMP transfer through LRRC8A/C volume-regulated anion channels 放疗通过LRRC8A/C容量调节阴离子通道通过cGAMP转移增强抗癌CD8 T细胞反应

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-27 DOI: 10.1126/sciimmunol.adn1630

Limin Cao, Li Wang, Zhihong Li, Xia Wei, Jinqiu Ding, Chun Zhou, Xia Chen, Zhicheng Huang, Zhugui Shao, Junchen Shen, Hongfei Lou, Keqing Zhao, Yuwei Huang, Yuanqin Yang, Han Liu, Yumeng Sun, Junling Niu, Shan Jiang, Rong Lu, Longhai Tang, Xiaoming Zhang, Haibing Zhang, Yichuan Xiao, Jianfeng Chen, Shixin Ma, Chengjiang Gao, Guangxun Meng, Li Liu, Zhaozhu Qiu, Haopeng Wang, Liufu Deng, Youqiong Ye, Xin-Ming Jia, Huabin Li, Hui Xiao

{"title":"Radiotherapy enhances anticancer CD8 T cell responses by cGAMP transfer through LRRC8A/C volume-regulated anion channels","authors":"Limin Cao, Li Wang, Zhihong Li, Xia Wei, Jinqiu Ding, Chun Zhou, Xia Chen, Zhicheng Huang, Zhugui Shao, Junchen Shen, Hongfei Lou, Keqing Zhao, Yuwei Huang, Yuanqin Yang, Han Liu, Yumeng Sun, Junling Niu, Shan Jiang, Rong Lu, Longhai Tang, Xiaoming Zhang, Haibing Zhang, Yichuan Xiao, Jianfeng Chen, Shixin Ma, Chengjiang Gao, Guangxun Meng, Li Liu, Zhaozhu Qiu, Haopeng Wang, Liufu Deng, Youqiong Ye, Xin-Ming Jia, Huabin Li, Hui Xiao","doi":"10.1126/sciimmunol.adn1630","DOIUrl":"10.1126/sciimmunol.adn1630","url":null,"abstract":"<div >The volume-regulated anion channels (VRACs) transport osmolytes, neurotransmitters, and cyclic GMP-AMP (cGAMP) across the cell membrane to regulate cell volume and host defense. We report that the leucine-rich repeat–containing 8A/C (LRRC8A/C) VRAC plays a crucial role in immune responses to radiotherapy and chemotherapy for cancer. VRACs transfer cGAMP from irradiated cancer cells to infiltrating CD4 and CD8 T cells, thus enhancing their effector functions. TCR signaling acts as a physiological signal to open the VRAC pore through phosphatidylinositol 4,5-bisphosphate [PI(4,5)P<sub>2</sub>] and reactive oxygen species (ROS). This allows the rapid uptake of cGAMP and STING activation in mouse and human T cells and induction of interferon-α/β, which up-regulate granzymes and IFN-γ in CD8 T cells. Inhibition of the extracellular hydroxylases CD39 and ENPP1 maintains extracellular ATP and cGAMP, which promotes VRAC-enhanced CD8 T cell anticancer function. Thus, the transfer of cGAMP to T cells by VRACs may be a strategy that can be targeted in future cancer therapies.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adn1630","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144500475","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

A Dock8-dependent mechanosensitive central actin pool maintains T cell shape and protects the nucleus during migration dock8依赖性的机械敏感的中央肌动蛋白池维持T细胞的形状并在迁移过程中保护细胞核

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-26 DOI: 10.1126/sciimmunol.adt9239

Connie Shen, Aysha Cerf, Jérémy Postat, Aanya Bhagrath, Mauricio Merino, Angela Mingarelli, Grace Barnes, Dhanesh Patel, Dakota Rogers, Vincent M. Luo, Afnan Abu-Thuraia, Caitlin Schneider, Daniela F. Quail, Abhinav Sharma, Woong-Kyung Suh, Allen Ehrlicher, Jean-François Côté, Judith N. Mandl

{"title":"A Dock8-dependent mechanosensitive central actin pool maintains T cell shape and protects the nucleus during migration","authors":"Connie Shen, Aysha Cerf, Jérémy Postat, Aanya Bhagrath, Mauricio Merino, Angela Mingarelli, Grace Barnes, Dhanesh Patel, Dakota Rogers, Vincent M. Luo, Afnan Abu-Thuraia, Caitlin Schneider, Daniela F. Quail, Abhinav Sharma, Woong-Kyung Suh, Allen Ehrlicher, Jean-François Côté, Judith N. Mandl","doi":"10.1126/sciimmunol.adt9239","DOIUrl":"10.1126/sciimmunol.adt9239","url":null,"abstract":"<div >Immune cells navigate through complex tissue architectures by extensive cellular deformation, low adhesion, and high cell velocities. Loss-of-function mutations in <i>dedicator of cytokinesis 8</i> (<i>Dock8</i>) are associated with immunodeficiency as immune cells becoming entangled during migration through dense environments, but their migration on two-dimensional surfaces remains entirely intact. Here, we investigated the specific cytoskeletal defect of <i>Dock8</i>-deficient activated T cells and describe a central pool of F-actin in wild-type murine and human T cells that is absent in <i>Dock8</i> knockout T cells. The appearance of the central actin pool is mechanoresponsive and emerges only when cells are very confined. We identified mammalian sterile 20-like (Mst1) as a necessary component in this mechanosensitive pathway in addition to Dock8, allowing for cell shape integrity and survival during migration through complex environments. Our work shows that loss of the central actin pool results in greater nuclear deformation, accrual of DNA damage, and premature cell senescence.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 109","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144488516","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

TNF switches homeostatic efferocytosis to lytic caspase-8–dependent pyroptosis and IL-1β maturation TNF将稳态efferocytosis转换为裂解caspase-8依赖性焦亡和IL-1β成熟

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-20 DOI: 10.1126/sciimmunol.adq0043

Hayley I. Muendlein, Wilson M. Connolly, Jamie Leiriao, Mei-An Nolan, Jennifer Judge, Irina Smirnova, Rebecca Batorsky, Alexander Poltorak

{"title":"TNF switches homeostatic efferocytosis to lytic caspase-8–dependent pyroptosis and IL-1β maturation","authors":"Hayley I. Muendlein, Wilson M. Connolly, Jamie Leiriao, Mei-An Nolan, Jennifer Judge, Irina Smirnova, Rebecca Batorsky, Alexander Poltorak","doi":"10.1126/sciimmunol.adq0043","DOIUrl":"10.1126/sciimmunol.adq0043","url":null,"abstract":"<div >Efferocytosis, wherein phagocytes engulf dead or dying cells, is a critical function of macrophages that supports cellular turnover, tissue repair, and resolution of inflammation. Despite its well-established anti-inflammatory mechanism in homeostasis, whether efferocytosis remains immunologically silent in the context of dysregulated immune responses such as sepsis or systemic inflammatory response syndrome (SIRS) has not been investigated. Here, we used mouse models of tumor necrosis factor (TNF)–induced SIRS and <i>Escherichia coli–</i>induced septic peritonitis to uncover a potential negative consequence of efferocytosis. We found that when activated with TNF, phagocytes efferocytosing neutrophils initiated a caspase-8–dependent, but NLRP3 inflammasome–independent, form of pyroptosis, which we termed “efferoptosis.” The maturation of IL-1β, a hallmark of pyroptotic cell death, also occurred independently of canonical inflammasome activation, supporting direct cleavage by caspase-8. Inhibition of efferocytosis protected mice against TNF-induced SIRS, suggesting that efferoptosis contributes to the pathology of sepsis and other TNF-mediated inflammatory conditions.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adq0043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329372","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

CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity CLNS1A调节基因组稳定性和细胞周期进程以控制CD4 T细胞功能和自身免疫

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-20 DOI: 10.1126/sciimmunol.adq8860

Liwei Wang, Lucile Noyer, Miki Jishage, Yin-Hu Wang, Anthony Y. Tao, Maxwell McDermott, Ivan Gando, Ikjot Sidhu, Ke Hu, Li Zhong, Katherine Sun, Dominik Drmic, Ulrike Kaufmann, Stefan Feske

{"title":"CLNS1A regulates genome stability and cell cycle progression to control CD4 T cell function and autoimmunity","authors":"Liwei Wang, Lucile Noyer, Miki Jishage, Yin-Hu Wang, Anthony Y. Tao, Maxwell McDermott, Ivan Gando, Ikjot Sidhu, Ke Hu, Li Zhong, Katherine Sun, Dominik Drmic, Ulrike Kaufmann, Stefan Feske","doi":"10.1126/sciimmunol.adq8860","DOIUrl":"10.1126/sciimmunol.adq8860","url":null,"abstract":"<div >Pathogenic CD4 T cells drive autoimmunity in diseases such as multiple sclerosis (MS) and inflammatory bowel disease (IBD). Through a forward genetic screen, we identified chloride nucleotide-sensitive channel 1A (CLNS1A) as a key regulator of inflammation in the experimental autoimmune encephalomyelitis (EAE) model of MS. CLNS1A is expressed in several subsets of CD4 T cells, including pathogenic T helper 17 (pT<sub>H</sub>17) cells. Deletion of <i>Clns1a</i> in T cells resulted in DNA damage, cell cycle arrest, impaired T cell proliferation, and effector function, thereby protecting mice from both EAE and IBD. We found that CLNS1A interacts with protein arginine methyl transferase 5 (PRMT5). Moreover, CLNS1A regulates symmetric histone dimethylation and the expression of genes involved in DNA repair, replication, and cell cycle progression. Thus, CLNS1A plays an important role in CD4 T cells by promoting genome stability and cell cycle progression.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329070","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 linear ontogeny accounts for the development of naive, memory, and tumor-infiltrating regulatory T cells in mice 线性个体发生解释了小鼠初始、记忆和肿瘤浸润调节性T细胞的发展

IF 17.6 1区医学

Science Immunology Pub Date : 2025-06-20 DOI: 10.1126/sciimmunol.adu7341

Sanmoy Pathak, Thea Hogan, Sanket Rane, Yundi Huang, Claire Pearson, Charles Sinclair, Simon Barry, Larissa Carnevalli, Andrew J. Yates, Benedict Seddon

{"title":"A linear ontogeny accounts for the development of naive, memory, and tumor-infiltrating regulatory T cells in mice","authors":"Sanmoy Pathak, Thea Hogan, Sanket Rane, Yundi Huang, Claire Pearson, Charles Sinclair, Simon Barry, Larissa Carnevalli, Andrew J. Yates, Benedict Seddon","doi":"10.1126/sciimmunol.adu7341","DOIUrl":"10.1126/sciimmunol.adu7341","url":null,"abstract":"<div >Regulatory T cells (T<sub>reg</sub> cells) are critical regulators of adaptive immunity and the pathophysiology of antitumoral immunity. T<sub>reg</sub> cells are both generated during thymic development and induced from peripheral conventional T cells. How these distinct pathways contribute to the homeostasis of circulating T<sub>reg</sub> cells in health and disease remains unclear. We addressed this question using multiple fate-mapping mouse systems and modeling. Naive and effector/memory (EM) T<sub>reg</sub> cells exhibit distinct dynamics but are both continuously replenished by de novo generation throughout life. The predominant precursors of circulating EM T<sub>reg</sub> cells are naive thymic T<sub>reg</sub> cells and not conventional T cells, a process driven by self rather than foreign antigen recognition. Using the same fate reporters and three tumor models, we demonstrate that infiltrating T<sub>reg</sub> cells specifically derive from preexisting EM T<sub>reg</sub> cells. In summary, we define a linear ontogeny of T<sub>reg</sub> cells from the thymus to EM, driven by self-antigen recognition, that then gives rise to tumor-infiltrating T<sub>reg</sub> cells.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144329373","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