Science Immunology最新文献

{"title":"Inflammatory mischief managed: How retinoic acid calms heart attacks at the (marrow) source","authors":"Sahily Reyes-Esteves,&nbsp;Christopher A. Hunter","doi":"10.1126/sciimmunol.adz3400","DOIUrl":"10.1126/sciimmunol.adz3400","url":null,"abstract":"<div >Targeting vitamin A metabolism limits emergency hematopoiesis and promotes resolution of inflammation in myocardial infarction.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232570","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}

{"title":"Inducible protein degradation reveals inflammation-dependent function of the Treg cell lineage–defining transcription factor Foxp3","authors":"Christina Jäger,&nbsp;Polina Dimitrova,&nbsp;Qiong Sun,&nbsp;Jesse Tennebroek,&nbsp;Elisa Marchiori,&nbsp;Markus Jaritz,&nbsp;Rene Rauschmeier,&nbsp;Guillem Estivill,&nbsp;Anna Obenauf,&nbsp;Meinrad Busslinger,&nbsp;Joris van der Veeken","doi":"10.1126/sciimmunol.adr7057","DOIUrl":"10.1126/sciimmunol.adr7057","url":null,"abstract":"<div >Regulatory T cells (T_reg cells) are immunosuppressive CD4 T cells defined by expression of the transcription factor Foxp3. Genetic loss-of-function mutations in <i>Foxp3</i> cause lethal multiorgan autoimmune inflammation resulting from defects in T_reg cell development and suppressive activity. Whether T_reg cells are continuously dependent on Foxp3 is still unclear. Here, we leveraged chemically induced protein degradation to show that functionally suppressive T_reg cells in healthy organs can persist in the near-complete absence of Foxp3 protein for at least 10 days. Conversely, T_reg cells responding to type 1 inflammation in settings of autoimmunity, viral infection, or cancer were selectively lost upon Foxp3 protein depletion. Acute degradation experiments revealed that Foxp3 acts mostly as a direct transcriptional repressor and modulates responsiveness to cytokine stimulation. This inflammation-dependent requirement for continuous Foxp3 activity enabled induction of a selective antitumor immune response upon systemic Foxp3 depletion, without causing deleterious T cell expansion in healthy organs.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232561","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}

{"title":"Immuno-amnesia: Without B cells, T cells cannot remember","authors":"Jonathan S. Maltzman","doi":"10.1126/sciimmunol.adz3620","DOIUrl":"10.1126/sciimmunol.adz3620","url":null,"abstract":"<div >Why B cells are needed for optimal CD8 T cell memory.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232592","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}

{"title":"An Il12 mRNA-LNP adjuvant enhances mRNA vaccine–induced CD8 T cell responses","authors":"Emily A. Aunins,&nbsp;Anthony T. Phan,&nbsp;Mohamad-Gabriel Alameh,&nbsp;Garima Dwivedi,&nbsp;Elisa Cruz-Morales,&nbsp;David A. Christian,&nbsp;Ying Tam,&nbsp;Molly E. Bunkofske,&nbsp;Anabel Zabala Peñafiel,&nbsp;Keenan M. O’Dea,&nbsp;Maria Merolle,&nbsp;Colleen Furey,&nbsp;Phillip Scott,&nbsp;Robert H. Vonderheide,&nbsp;Scott E. Hensley,&nbsp;Ross M. Kedl,&nbsp;Drew Weissman,&nbsp;Christopher A. Hunter","doi":"10.1126/sciimmunol.ads1328","DOIUrl":"10.1126/sciimmunol.ads1328","url":null,"abstract":"<div >Optimizing vaccine design to induce CD8 T cell responses has been challenging, but lipid nanoparticle (LNP)–encapsulated mRNA vaccines effectively generate CD8 T cell memory. Interleukin-12 (IL-12) supports CD8 T cell expansion and acquisition of effector function, but the role of IL-12 in the generation of CD8 T responses to mRNA vaccination is unclear. Here, we determine that endogenous IL-12 is not required for CD8 T cell responses to mRNA-LNP vaccination. We assessed the adjuvant activity of an mRNA-LNP encapsulating a codon-optimized mRNA that encodes both subunits of IL-12 (LNP–IL-12). Coadministration of LNP–IL-12 with ovalbumin (OVA) mRNA-LNPs enhanced CD8 T cell expansion and effector function and expanded circulating, effector, and tissue-resident memory CD8 T cells. LNP–IL-12 increased CD8 T cell responses against SARS-CoV-2 and influenza virus antigens and improved protection against <i>Listeria monocytogenes</i>–OVA and B16F0-OVA melanoma. Thus, modification of mRNA-LNP formulations to include a cytokine mRNA provides a strategy to enhance CD8 T cell–mediated protection.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads1328","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232586","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}

{"title":"Dissection of the immune landscape in psoriatic arthritis defines immunoproteasome up-regulation in treatment resistance","authors":"Reut Tzemach,&nbsp;Chamutal Gur,&nbsp;Truong San Phan,&nbsp;Eyal David,&nbsp;Mor Zada,&nbsp;Merav D. Shmueli,&nbsp;Kfir Mazuz,&nbsp;Fadi Sheban,&nbsp;Anna Kurilovich,&nbsp;Maya Ben Yehuda,&nbsp;Victoria Furer,&nbsp;Ari Polachek,&nbsp;Smadar Gertel,&nbsp;Nimrod Snir,&nbsp;Tali Eviatar,&nbsp;Sharon Nevo,&nbsp;Yifat Merbl,&nbsp;Daphna Paran,&nbsp;Shuang-Yin Wang,&nbsp;Ori Elkayam,&nbsp;Ido Amit","doi":"10.1126/sciimmunol.adu0284","DOIUrl":"10.1126/sciimmunol.adu0284","url":null,"abstract":"<div >Despite substantial advancements in psoriatic arthritis (PsA) treatment modalities, a considerable proportion of patients continue to experience persistent joint inflammation, unresponsive to the armamentarium of disease-modifying antirheumatic drugs. Identifying previously unknown biomarkers and targets for refractory disease is urgently needed. Here, using single-cell RNA sequencing of synovial fluid from 41 patients with PsA and 9 osteoarthritis (OA) controls, we mapped the immune landscape of the pathogenic synovial fluid in patients with PsA. Our analysis revealed profound alterations in the myeloid compartment, primarily in type 2 conventional dendritic cells and monocytes. A comparison of these myeloid programs in PsA patient groups identified elevated expression of genes associated with the immunoproteasome and major histocompatibility complex class I as a major perturbation in refractory patients. Functional in vivo and in vitro experiments using a selective immunoproteasome inhibitor attenuated the activated myeloid compartment and disease manifestations. Our research imparts critical insights into PsA pathogenesis, potentially paving a way for targeted therapeutic interventions in treatment-resistant patients.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 108","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adu0284","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232600","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}

{"title":"Human LY9 governs CD4+ T cell IFN-γ immunity to Mycobacterium tuberculosis","authors":"Masato Ogishi,&nbsp;Julia Puchan,&nbsp;Rui Yang,&nbsp;Andrés Augusto Arias,&nbsp;Ji Eun Han,&nbsp;Tina Nguyen,&nbsp;Rebeca Gutiérrez-Cózar,&nbsp;Clément Conil,&nbsp;Yoann Seeleuthner,&nbsp;Darawan Rinchai,&nbsp;Peng Zhang,&nbsp;Khoren Ponsin,&nbsp;Matthieu Chaldebas,&nbsp;Yi Feng,&nbsp;Anna-Lena Neehus,&nbsp;Ottavia M. Delmonte,&nbsp;Taushif Khan,&nbsp;Nils Landegren,&nbsp;Daniel Eriksson,&nbsp;Jonathan Bohlen,&nbsp;Jessica N. Peel,&nbsp;Iris Fagniez,&nbsp;Simon J. Pelham,&nbsp;Wei-Te Lei,&nbsp;Maya Chrabieh,&nbsp;Candice Laine,&nbsp;Hind Ouair,&nbsp;Ibtihal Benhsaien,&nbsp;Ahmed Abid,&nbsp;Ismail Abderrhamani Ghorfi,&nbsp;Hicham Souhi,&nbsp;Hanane Ouazzani,&nbsp;Rafik Aniss,&nbsp;D. Sean Riminton,&nbsp;Olle Kämpe,&nbsp;Stuart E. Turvey,&nbsp;Nico Marr,&nbsp;Luigi D. Notarangelo,&nbsp;Nevin Hatipoglu,&nbsp;Aziz Bousfiha,&nbsp;Tayfun Ozcelik,&nbsp;Jamila El Baghdadi,&nbsp;Aurelie Cobat,&nbsp;Cindy S. Ma,&nbsp;Laurent Abel,&nbsp;Anne Puel,&nbsp;Jacinta Bustamante,&nbsp;Pablo Engel,&nbsp;Philippe Gros,&nbsp;Stuart G. Tangye,&nbsp;Federica Sallusto,&nbsp;Stéphanie Boisson-Dupuis,&nbsp;Jean-Laurent Casanova","doi":"10.1126/sciimmunol.ads7377","DOIUrl":"10.1126/sciimmunol.ads7377","url":null,"abstract":"<div >CD4⁺ T cells are indispensable for optimal immunity to <i>Mycobacterium tuberculosis</i> (<i>M.tb</i>), a pathogen that triggers tuberculosis (TB) in humans. <i>M.tb</i>-specific human CD4⁺ T cells are known to polarize toward an interferon-γ (IFN-γ)–producing, CCR4⁻CCR6⁺CXCR3⁺T-bet⁺RORγT⁺ T helper 1* cell (T_H1*cell) memory phenotype. We report that autosomal recessive deficiency of the human lymphocytic surface receptor LY9 (SLAMF3 and CD229), which is found in less than 10⁻⁵ individuals in the general population, underlies TB in three unrelated patients due to selective impairment in IFN-γ production by T_H1* cells. T_H1* cells express higher levels of LY9 than other CD4⁺ T cells. Mechanistically, LY9 polarizes naïve CD4⁺ T cells toward memory T_H1* cells by inducing T-bet via signaling lymphocytic activation molecule (SLAM)–associated protein (SAP) and RORγT (thymus-specific retinoid-related orphan receptor γ) without SAP. LY9 costimulation enhances TCR-driven IFN-γ production of memory T_H1*, but not T_H1, cells in a T cell–intrinsic manner via NFAT1 (nuclear factor of activated T cells 1) and RORγT. LY9 is likely to govern an optimal T_H1* cell– and IFN-γ–dependent protective immunity to <i>M.tb</i> in humans.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads7377","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179428","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}

{"title":"An activating Stat1 mutant disrupts normal STAT4 innate lymphocyte programs during viral infection","authors":"Rachael L. Philips,&nbsp;Yi-Chu Liao,&nbsp;Colleen M. Lau,&nbsp;Tasha A. Morrison,&nbsp;Kan Jiang,&nbsp;Amal Hutchinson,&nbsp;Justin Shayne,&nbsp;Chen Yao,&nbsp;Joseph C. Sun,&nbsp;Heather D. Hickman,&nbsp;Joshua D. Milner,&nbsp;Steve Holland,&nbsp;Yuka Kanno,&nbsp;Michail S. Lionakis,&nbsp;John J. O’Shea","doi":"10.1126/sciimmunol.ado5986","DOIUrl":"10.1126/sciimmunol.ado5986","url":null,"abstract":"<div >Interferonopathies drive autoimmunity but can also impair host responses to pathogens, including viral infections. To better understand viral susceptibility of patients with <i>STAT1</i> gain-of-function (GOF) mutations, we generated conditional knockin mouse models to elucidate disease mechanisms and relevance of different immune subsets. Virally infected <i>Stat1</i> GOF mice exhibited impaired early IFN-γ production from innate lymphocytes and lethality because of excess prolonged multicytokine production. The presence of the <i>Stat1</i> GOF allele resulted in premature usage of interferon-stimulated gene factor 3 (ISGF3) over the normal STAT4–AP-1–dependent transcriptomic program in activated innate lymphocytes. Administration of anti–IFN-γ antibodies in wild-type (WT) mice after infection phenocopied <i>Stat1</i> GOF mice presenting exaggerated inflammation despite viral control. Conversely, early administration of exogenous IFN-γ to infected <i>Stat1</i> GOF mice prevented lethality and exaggerated cytokine response. Although <i>Stat1</i> GOF mutations facilitate IFN-γ–mediated autoimmunity, early IFN-γ responses to viral infection via a normal STAT4 program were impaired, leading to overcompensated inflammatory responses in <i>Stat1</i> GOF mice.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144179456","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}

{"title":"A light-regulated circadian timer optimizes neutrophil bactericidal activity to boost daytime immunity","authors":"Lucia Yi Du,&nbsp;Pramuk Keerthisinghe,&nbsp;Leah Rolland,&nbsp;Yih Jian Sung,&nbsp;Hannah Darroch,&nbsp;Tanja Linnerz,&nbsp;Elina Ashimbayeva,&nbsp;Matthew J. Grant,&nbsp;Purvi M. Kakadia,&nbsp;Annasuya Ramachandran,&nbsp;Alexander Tups,&nbsp;Herman P. Spaink,&nbsp;Stefan K. Bohlander,&nbsp;James Cheeseman,&nbsp;Philip S. Crosier,&nbsp;Jonathan W. Astin,&nbsp;Guy Warman,&nbsp;Christopher J. Hall","doi":"10.1126/sciimmunol.adn3080","DOIUrl":"10.1126/sciimmunol.adn3080","url":null,"abstract":"<div >The immune response exhibits strong circadian rhythmicity, with enhanced bacterial clearance often synchronized with an organism’s active phase. Despite providing the bulk of cellular antibacterial defense, the neutrophil clockwork is poorly understood. Here, we used larval zebrafish to explore the role of clock genes in neutrophils during infection. <i>Per2</i> was required in neutrophils for reactive oxygen species (ROS) production and bacterial killing by enhancing infection-responsive expression of <i>high-mobility group box 1a</i> (<i>hmgb1a</i>). The Cry binding domain of Per2 was required for regulation of neutrophil bactericidal activity, and neutrophils lacking Cry1a had elevated bactericidal activity and infection-responsive <i>hmgb1a</i> expression. A conserved cis-regulatory element with BMAL1 and nuclear factor κB binding motifs gated infection-responsive <i>hmgb1a</i> expression to the light phase. Mutagenesis of the BMAL1 motif in neutrophils blunted the priming effect of light on bactericidal activity and <i>hmgb1a</i> expression. These findings identify a light-responsive cell-intrinsic timer that controls time-of-day variations in antibacterial activity.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.adn3080","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122949","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}

{"title":"An engineered viral protein activates STAT5 to prevent T cell suppression","authors":"Yating Zheng,&nbsp;Zehui Gu,&nbsp;Claire E. Shudde,&nbsp;Taylor L. Piper,&nbsp;Xinyu Wang,&nbsp;Grace A. Aleck,&nbsp;Jiajia Zhou,&nbsp;Dana King,&nbsp;Monica K. Chanda,&nbsp;Lilliana Trinch,&nbsp;Weiping Zou,&nbsp;Adam H. Courtney","doi":"10.1126/sciimmunol.adn9633","DOIUrl":"10.1126/sciimmunol.adn9633","url":null,"abstract":"<div >T cell therapy efficacy can be compromised if cytokine-induced Janus kinase (JAK)–signal transducer and activator of transcription (STAT) signaling is dysregulated or insufficient to sustain functionality. Here, we demonstrate that LCK kinase activity can be recruited to noncanonical protein substrates to directly activate targeted STAT proteins in T cells. STAT activation was accomplished by engineering the herpesvirus saimiri tyrosine kinase interacting protein (TIP) to provide a platform for the enforced recruitment of LCK to STAT proteins. We determined that a minimal region of TIP that binds to LCK could be combined with STAT binding sites derived from endogenous cytokine receptors. These constructs activated targeted STAT proteins in a cytokine-independent manner. We identified a STAT5 activator that sustained CD8+ T cell survival and cytotoxic function ex vivo in the absence of interleukin-2. Tumor outgrowth was reduced in vivo because of enhanced T cell persistence and functionality. Single-cell transcriptomics revealed that the STAT5 activator prevented the expression of genes associated with an exhausted T cell fate. Our findings demonstrate that signaling pathways can be rewired in T cells to sustain their function in solid tumors.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144122798","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}

{"title":"C/EBPα activates Irf8 expression in myeloid progenitors at the +56-kb enhancer to initiate cDC1 development","authors":"Jing Chen,&nbsp;Tian-Tian Liu,&nbsp;Feiya Ou,&nbsp;Ray A. Ohara,&nbsp;Suin Jo,&nbsp;Joshua Luke Postoak,&nbsp;Takeshi Egawa,&nbsp;Ryan B. Day,&nbsp;Theresa L. Murphy,&nbsp;Kenneth M. Murphy,&nbsp;Sunkyung Kim","doi":"10.1126/sciimmunol.adt5899","DOIUrl":"10.1126/sciimmunol.adt5899","url":null,"abstract":"<div >Development of type 1 conventional dendritic cells (cDC1s) underlies the capacity to generate antiviral and antitumor immune responses. Here, we identify the basis for cDC1 development from its earliest progenitors, determining the hierarchy of several required transcription factors and uncovering a series of mandatory cis interactions between constituent enhancers within the <i>Irf8</i> superenhancer. We produced in vivo mutations of two C/EBPα binding sites that comprise the <i>Irf8</i> +56–kilobase (kb) enhancer that markedly reduced IRF8 expression in all myeloid progenitors and impaired cDC1 development. These sites did not bind RUNX1 or RUNX3, and C/EBPα expression was instead regulated by their action at the <i>Cebpa</i> +37-kb enhancer, placing RUNX factors upstream of <i>Cebpa</i> in regulating <i>Irf8</i>. Last, we demonstrate that cis interactions between the +56-kb <i>Irf8</i> enhancer and the previously reported +41- and +32-kb <i>Irf8</i> enhancers are mandatory in the sequential progression of these stage-specific constituent elements.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144067020","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}