Pub Date : 2025-12-12DOI: 10.1126/sciimmunol.aed8718
{"title":"Erratum for the Review “The immunology of brain tumors” by L. Bunse et al.","authors":"","doi":"10.1126/sciimmunol.aed8718","DOIUrl":"10.1126/sciimmunol.aed8718","url":null,"abstract":"","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145730623","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}
Pub Date : 2025-12-05DOI: 10.1126/sciimmunol.adw9903
Anna Czarkwiani, Macrina Lobo, Lizbeth Airais Bolaños Castro, Andreas Petzold, Fabian Rost, René Maehr, Maximina H. Yun
The thymus is the primary site of T cell development, central to the establishment of self-tolerance and adaptive immune function. In mammals, the thymus undergoes age-related involution, resulting in a global decline in immune function. The thymus has some regenerative ability that relies on pre-existing thymic remnants but is insufficient to prevent involution. Here, we show that the juvenile axolotl (Ambystoma mexicanum) is able to regenerate its thymus de novo after complete removal, constituting an exception among vertebrates. Using single-cell transcriptomics and genetic and transplantation approaches, we demonstrate that de novo thymus regeneration results in the restoration of morphology, cell-type diversity, and function. FOXN1, although it has a conserved role in thymus organogenesis, is dispensable for the initiation of thymic regeneration. In contrast, we identify midkine signaling as a possible early driver of de novo thymus regeneration. This study demonstrates an instance of organ-level regeneration of the lymphoid system, which could guide future clinical strategies seeking to promote thymus regrowth.
{"title":"Molecular basis for de novo thymus regeneration in a vertebrate, the axolotl","authors":"Anna Czarkwiani, Macrina Lobo, Lizbeth Airais Bolaños Castro, Andreas Petzold, Fabian Rost, René Maehr, Maximina H. Yun","doi":"10.1126/sciimmunol.adw9903","DOIUrl":"10.1126/sciimmunol.adw9903","url":null,"abstract":"<div >The thymus is the primary site of T cell development, central to the establishment of self-tolerance and adaptive immune function. In mammals, the thymus undergoes age-related involution, resulting in a global decline in immune function. The thymus has some regenerative ability that relies on pre-existing thymic remnants but is insufficient to prevent involution. Here, we show that the juvenile axolotl (<i>Ambystoma mexicanum</i>) is able to regenerate its thymus de novo after complete removal, constituting an exception among vertebrates. Using single-cell transcriptomics and genetic and transplantation approaches, we demonstrate that de novo thymus regeneration results in the restoration of morphology, cell-type diversity, and function. FOXN1, although it has a conserved role in thymus organogenesis, is dispensable for the initiation of thymic regeneration. In contrast, we identify midkine signaling as a possible early driver of de novo thymus regeneration. This study demonstrates an instance of organ-level regeneration of the lymphoid system, which could guide future clinical strategies seeking to promote thymus regrowth.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adw9903","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145674527","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}
Pub Date : 2025-12-05DOI: 10.1126/sciimmunol.aee1941
Dachuan Dong, Jonathan S. Maltzman
Deletion of the SPPL3 sheddase improves allogeneic CAR T cell persistence.
删除SPPL3脱落酶可改善同种异体CAR - T细胞的持久性。
{"title":"Sugar-coated CAR T for sweeter cell therapies","authors":"Dachuan Dong, Jonathan S. Maltzman","doi":"10.1126/sciimmunol.aee1941","DOIUrl":"10.1126/sciimmunol.aee1941","url":null,"abstract":"<div >Deletion of the SPPL3 sheddase improves allogeneic CAR T cell persistence.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145675757","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}
Pub Date : 2025-12-05DOI: 10.1126/sciimmunol.aee1940
Thomas T. Xu, Shiv Pillai
Antibodies against specific epitopes were designed with assistance from artificial intelligence.
针对特定表位的抗体是在人工智能的帮助下设计的。
{"title":"Smart chains: Designer antibodies shaped by AI","authors":"Thomas T. Xu, Shiv Pillai","doi":"10.1126/sciimmunol.aee1940","DOIUrl":"10.1126/sciimmunol.aee1940","url":null,"abstract":"<div >Antibodies against specific epitopes were designed with assistance from artificial intelligence.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145675758","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}
Pub Date : 2025-12-05DOI: 10.1126/sciimmunol.adx1794
Lucie Rodriguez-Coffinet, Dmitri Kazmin, Bali Pulendran
The advent of large language models (LLMs) has transformed academic research by accelerating hypothesis generation and data analysis. LLMs can help researchers uncover patterns and insights from vast datasets to foster innovative scientific discovery. However, questions arise regarding the creative capacity of artificial intelligence (AI), especially in biologically complex fields such as vaccinology. This study evaluates the ability of LLMs to generate hypotheses, design experiments, and infer broader biological principles through a proposed framework called “The Creation Game.” Using three case studies—general control nonderepressible 2 (GCN2)’s role in dendritic cell antigen presentation via stress response, sterol regulatory element–binding protein (SREBP)’s influence on metabolic responses, and Toll-like receptor 5 (TLR5)’s connection to microbiota-driven vaccine efficacy—we assessed AI’s accuracy, logic, and creativity. The findings underscore the potential of LLMs to accelerate vaccine research while emphasizing the importance of ethical oversight. By complementing human creativity, AI could potentially transform hypothesis-driven science, paving the way for tailored vaccination strategies and deeper insights into human immunity.
{"title":"Assessing AI’s cognitive abilities for scientific discovery in the field of systems vaccinology","authors":"Lucie Rodriguez-Coffinet, Dmitri Kazmin, Bali Pulendran","doi":"10.1126/sciimmunol.adx1794","DOIUrl":"10.1126/sciimmunol.adx1794","url":null,"abstract":"<div >The advent of large language models (LLMs) has transformed academic research by accelerating hypothesis generation and data analysis. LLMs can help researchers uncover patterns and insights from vast datasets to foster innovative scientific discovery. However, questions arise regarding the creative capacity of artificial intelligence (AI), especially in biologically complex fields such as vaccinology. This study evaluates the ability of LLMs to generate hypotheses, design experiments, and infer broader biological principles through a proposed framework called “The Creation Game.” Using three case studies—general control nonderepressible 2 (GCN2)’s role in dendritic cell antigen presentation via stress response, sterol regulatory element–binding protein (SREBP)’s influence on metabolic responses, and Toll-like receptor 5 (TLR5)’s connection to microbiota-driven vaccine efficacy—we assessed AI’s accuracy, logic, and creativity. The findings underscore the potential of LLMs to accelerate vaccine research while emphasizing the importance of ethical oversight. By complementing human creativity, AI could potentially transform hypothesis-driven science, paving the way for tailored vaccination strategies and deeper insights into human immunity.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adx1794","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145674523","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}
Pub Date : 2025-12-05DOI: 10.1126/sciimmunol.aea8735
Jacob Kim, Ao Huang, John S. Tsang
Large language model (LLM)–based artificial intelligence (AI) agents are powerful tools that can help researchers automate complex tasks such as literature review, data mining, computational code generation, and summarization of existing knowledge, but they can still fall short in developing original biological hypotheses and insights (see related Research Article by Rodriguez-Coffinet et al. in this issue). Emerging advances in multiagent systems and human-agent collaborative frameworks offer promising steps forward.
基于大型语言模型（LLM）的人工智能（AI）代理是一种强大的工具，可以帮助研究人员自动完成复杂的任务，如文献综述、数据挖掘、计算代码生成和现有知识的总结，但它们在开发原始生物学假设和见解方面仍然存在不足（参见Rodriguez-Coffinet et al.在本期的相关研究文章）。多智能体系统和人类智能体协作框架的新进展提供了有希望的进步。
{"title":"AI immunologists are here: Are they ready for prime time?","authors":"Jacob Kim, Ao Huang, John S. Tsang","doi":"10.1126/sciimmunol.aea8735","DOIUrl":"10.1126/sciimmunol.aea8735","url":null,"abstract":"<div >Large language model (LLM)–based artificial intelligence (AI) agents are powerful tools that can help researchers automate complex tasks such as literature review, data mining, computational code generation, and summarization of existing knowledge, but they can still fall short in developing original biological hypotheses and insights (see related Research Article by Rodriguez-Coffinet <i>et al.</i> in this issue). Emerging advances in multiagent systems and human-agent collaborative frameworks offer promising steps forward.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 114","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145674552","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}
Pub Date : 2025-11-28DOI: 10.1126/sciimmunol.adz4626
Elisabeth De Leeuw, Josefine F. Justesen, Cédric Bosteels, Nincy Debeuf, Manon Vanheerswynghels, Leander Jonckheere, Caroline De Wolf, Alysia Wayenberg, Karel F.A. Van Damme, Stijn Vanhee, Manon Lesage, Kim Deswarte, Sam Dupont, Morten Dahl, Hamida Hammad, Bart N. Lambrecht
Allergic asthma arises from complex genetic and environmental interactions. Analysis of a population-wide registry revealed that infants hospitalized for human respiratory syncytial virus (RSV) bronchiolitis who are born to asthmatic parents have a markedly increased risk of developing asthma. To model this interaction, neonatal mice infected with pneumonia virus of mice (PVM), an RSV analog, before house dust mite (HDM) exposure developed amplified type 2 inflammation and asthma-like pathology. Maternal, but not paternal, HDM allergy intensified disease, implicating vertical transmission of an immune risk factor. Mechanistically, neonatal viral infection up-regulated Fc receptors (FcRs) and promoted maturation of type 2 conventional dendritic cells (cDC2s). Maternal allergen-specific immunoglobulin G (IgG), transferred via neonatal Fc receptor (FcRn), enhanced Fc gamma receptor (FcγR)–mediated allergen uptake and T helper 2 (TH2) cell priming. Preventive RSV immunoprophylaxis blocked asthma development in this setting. These findings identify maternal allergy and neonatal RSV infection as converging FcR-dependent causal asthma risk factors, preventable through immunoprophylaxis.
{"title":"Maternal allergy and neonatal RSV infection synergize via FcR-mediated allergen uptake to promote the development of asthma in early life","authors":"Elisabeth De Leeuw, Josefine F. Justesen, Cédric Bosteels, Nincy Debeuf, Manon Vanheerswynghels, Leander Jonckheere, Caroline De Wolf, Alysia Wayenberg, Karel F.A. Van Damme, Stijn Vanhee, Manon Lesage, Kim Deswarte, Sam Dupont, Morten Dahl, Hamida Hammad, Bart N. Lambrecht","doi":"10.1126/sciimmunol.adz4626","DOIUrl":"10.1126/sciimmunol.adz4626","url":null,"abstract":"<div >Allergic asthma arises from complex genetic and environmental interactions. Analysis of a population-wide registry revealed that infants hospitalized for human respiratory syncytial virus (RSV) bronchiolitis who are born to asthmatic parents have a markedly increased risk of developing asthma. To model this interaction, neonatal mice infected with pneumonia virus of mice (PVM), an RSV analog, before house dust mite (HDM) exposure developed amplified type 2 inflammation and asthma-like pathology. Maternal, but not paternal, HDM allergy intensified disease, implicating vertical transmission of an immune risk factor. Mechanistically, neonatal viral infection up-regulated Fc receptors (FcRs) and promoted maturation of type 2 conventional dendritic cells (cDC2s). Maternal allergen-specific immunoglobulin G (IgG), transferred via neonatal Fc receptor (FcRn), enhanced Fc gamma receptor (FcγR)–mediated allergen uptake and T helper 2 (T<sub>H</sub>2) cell priming. Preventive RSV immunoprophylaxis blocked asthma development in this setting. These findings identify maternal allergy and neonatal RSV infection as converging FcR-dependent causal asthma risk factors, preventable through immunoprophylaxis.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 113","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adz4626","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145613130","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}
Pub Date : 2025-11-21DOI: 10.1126/sciimmunol.aed4813
Seth Thomas Scanlon
{"title":"Editorial expression of concern","authors":"Seth Thomas Scanlon","doi":"10.1126/sciimmunol.aed4813","DOIUrl":"10.1126/sciimmunol.aed4813","url":null,"abstract":"","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 113","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145561891","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}
Pub Date : 2025-11-21DOI: 10.1126/sciimmunol.adz0472
Maryam Abedi, Priyadarshini Rai, Yeqiao Zhou, Chengyang Liu, Isabelle Johnson, Aditi Chandra, Maria Fasolino, Susan Rostami, Wei Wang, Zaw Min, Yanjing Li, Ming Yu, Atishay Jay, Vung Lian, Michael Silverman, Klaus H. Kaestner, Ali Naji, Robert B. Faryabi, Golnaz Vahedi
Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β cells in the pancreas. While current therapies focus on managing the disease, a deeper understanding of the underlying molecular mechanisms is crucial for developing disease-modifying interventions. In this study, we conducted a comprehensive analysis of gene expression and chromatin accessibility in nearly 1 million immune cells from the pancreatic lymph nodes and spleens of 43 individuals with and without T1D. We found a distinct subset of CD4 T cells specifically present in the pancreatic lymph nodes of organ donors representing the active disease stage. These cells exhibited elevated activity of NFKB1 and BACH2, along with extensive chromatin remodeling associated with these transcription factors, which we also corroborated in a mouse model of T1D. A better understanding of these NFKB1-BACH2–expressing CD4 T cells may lead to therapeutic avenues for preventing or delaying T1D onset.
{"title":"Joint profiling of gene expression and chromatin accessibility in pancreatic lymph nodes and spleens in human type 1 diabetes","authors":"Maryam Abedi, Priyadarshini Rai, Yeqiao Zhou, Chengyang Liu, Isabelle Johnson, Aditi Chandra, Maria Fasolino, Susan Rostami, Wei Wang, Zaw Min, Yanjing Li, Ming Yu, Atishay Jay, Vung Lian, Michael Silverman, Klaus H. Kaestner, Ali Naji, Robert B. Faryabi, Golnaz Vahedi","doi":"10.1126/sciimmunol.adz0472","DOIUrl":"10.1126/sciimmunol.adz0472","url":null,"abstract":"<div >Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of insulin-producing β cells in the pancreas. While current therapies focus on managing the disease, a deeper understanding of the underlying molecular mechanisms is crucial for developing disease-modifying interventions. In this study, we conducted a comprehensive analysis of gene expression and chromatin accessibility in nearly 1 million immune cells from the pancreatic lymph nodes and spleens of 43 individuals with and without T1D. We found a distinct subset of CD4 T cells specifically present in the pancreatic lymph nodes of organ donors representing the active disease stage. These cells exhibited elevated activity of <i>NFKB1</i> and <i>BACH2</i>, along with extensive chromatin remodeling associated with these transcription factors, which we also corroborated in a mouse model of T1D. A better understanding of these <i>NFKB1-BACH2</i>–expressing CD4 T cells may lead to therapeutic avenues for preventing or delaying T1D onset.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 113","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adz0472","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145559336","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}
Pub Date : 2025-11-21DOI: 10.1126/sciimmunol.adu2089
Han Feng, Sungjun Park, Jae Woo Shin, Francisco Emmanuel Castañeda-Castro, Job Rocha Hernandez, Benjamin J. Schmiedel, Changlu Liu, Michael R. Jackson, Christian H. Ottensmeier, Pandurangan Vijayanand
Tissue-resident memory CD8 T (TRM) cells provide critical antiviral and antitumor immunity, but the molecular pathways guiding their development are not fully defined. Here, we identify the G protein–coupled receptor GPR25, induced by TGF-β signaling, as a regulator of TRM cell formation. Using adoptive transfer, we found that Gpr25-deficient T cells infiltrated tissues normally after viral infection but failed to efficiently develop into TRM cells. In a tumor challenge model, Gpr25 deficiency impaired TRM cell expansion and tumor control. Single-cell transcriptomics revealed defective acquisition of stem-like TRM cell features, including expression of T cell factor 1 (TCF1). After antigen rechallenge, Gpr25-deficient TRM cells showed impaired secondary TRM cell differentiation and maintenance. Moreover, Gpr25-deficient T cells displayed negative enrichment of TGF-β signature genes and impaired responses to TGF-β, indicating that GPR25 enhances TGF-β signaling to promote TRM cell development. Our findings suggest that modulating GPR25 function may provide a therapeutic strategy to improve TRM cell responses in infection and cancer.
{"title":"GPR25 promotes the formation of lung and liver tissue-resident memory CD8 T cells","authors":"Han Feng, Sungjun Park, Jae Woo Shin, Francisco Emmanuel Castañeda-Castro, Job Rocha Hernandez, Benjamin J. Schmiedel, Changlu Liu, Michael R. Jackson, Christian H. Ottensmeier, Pandurangan Vijayanand","doi":"10.1126/sciimmunol.adu2089","DOIUrl":"10.1126/sciimmunol.adu2089","url":null,"abstract":"<div >Tissue-resident memory CD8 T (T<sub>RM</sub>) cells provide critical antiviral and antitumor immunity, but the molecular pathways guiding their development are not fully defined. Here, we identify the G protein–coupled receptor GPR25, induced by TGF-β signaling, as a regulator of T<sub>RM</sub> cell formation. Using adoptive transfer, we found that <i>Gpr25</i>-deficient T cells infiltrated tissues normally after viral infection but failed to efficiently develop into T<sub>RM</sub> cells. In a tumor challenge model, <i>Gpr25</i> deficiency impaired T<sub>RM</sub> cell expansion and tumor control. Single-cell transcriptomics revealed defective acquisition of stem-like T<sub>RM</sub> cell features, including expression of T cell factor 1 (TCF1). After antigen rechallenge, <i>Gpr25</i>-deficient T<sub>RM</sub> cells showed impaired secondary T<sub>RM</sub> cell differentiation and maintenance. Moreover, <i>Gpr25</i>-deficient T cells displayed negative enrichment of TGF-β signature genes and impaired responses to TGF-β, indicating that GPR25 enhances TGF-β signaling to promote T<sub>RM</sub> cell development. Our findings suggest that modulating GPR25 function may provide a therapeutic strategy to improve T<sub>RM</sub> cell responses in infection and cancer.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 113","pages":""},"PeriodicalIF":16.3,"publicationDate":"2025-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145559340","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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