Journal of immunology最新文献

{"title":"Skullcapflavone II alleviates osteoarthritis by inhibiting inflammation and ferroptosis via the SLC7A11/GPX4 signaling pathway.","authors":"Jianing Lu, Yijun Lian, Qingchao Ru, Xin Guo, Bowen Han, Yang Liu","doi":"10.1093/jimmun/vkag230","DOIUrl":"https://doi.org/10.1093/jimmun/vkag230","url":null,"abstract":"<p><p>Osteoarthritis (OA), the most prevalent degenerative joint disease, leads to significant disability in the elderly and is characterized by functional and structural deterioration of the knee joint. This study aimed to investigate the therapeutic potential of skullcapflavone II (SkII), a flavonoid known for its anti-inflammatory properties, in the context of OA. Our results demonstrated that SkII markedly suppressed IL-1β-induced extracellular matrix degradation and apoptosis in chondrocytes. Furthermore, SkII reduced reactive oxygen species and malondialdehyde levels while enhancing superoxide dismutase activity and the glutathione/glutathione disulfide ratio. SkII also upregulated the expression of SLC7A11 and glutathione peroxidase 4 (GPX4). Mechanistic investigations revealed that SkII, similar to the ferroptosis inhibitor ferrostatin-1, effectively counteracted erastin-induced apoptosis and extracellular matrix degradation. Both SkII and ferrostatin-1 promoted SLC7A11 and GPX4 expression at transcriptional and protein levels and diminished ferrous ion (Fe2+) accumulation in chondrocytes. In vivo experiments confirmed that SkII treatment attenuated ferroptosis in OA rats by activating the SLC7A11/GPX4 pathway. In conclusion, our findings indicate that SkII alleviates OA progression by inhibiting ferroptosis through the SLC7A11/GPX4 signaling axis. These results underscore the potential of SkII as a promising therapeutic candidate for the treatment and prevention of OA.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a regulatory allosteric site in Arid5a unveils a therapeutic axis for systemic inflammation.","authors":"Hamza Hanieh, Hozaifa Metwally, Tadamitsu Kishimoto","doi":"10.1093/jimmun/vkag215","DOIUrl":"https://doi.org/10.1093/jimmun/vkag215","url":null,"abstract":"<p><p>Adenine-thymine (AT)-rich interactive domain-containing protein 5a (Arid5a) is an RNA-binding protein (RBP) that post-transcriptionally stabilizes mRNAs encoding proinflammatory mediators, including Interleukin-6 (IL-6), thereby amplifying inflammation. However, structural basis and regulatory mechanisms of Arid5a function remain poorly defined. In this study, we identified and characterized a conserved allosteric site within the ARID domain that regulates Arid5a-mediated mRNA stabilization. Using integrative in silico modeling and in vitro assays, 2 picolinamide-based inhibitors, NFP1 and NFP2, were designed to specifically engage the allosteric site constituent residues. Mutational and functional analyses revealed Tyr88 and Val91 as key regulatory elements within the allosteric site, essential for transmitting conformational regulation upon ligand engagement. Pharmacological inhibition of the allosteric site disrupted Arid5a interaction with target RNA stem-loop structure, reduced stability of Il6 mRNA, and attenuated inflammatory responses in Lipopolysaccharide (LPS)-stimulated macrophages. Furthermore, Arid5a inhibitors reduced the stability of other target mRNAs, including Signal transducer and activator of transcription 3 (Stat3) and OX40, in polarized T helper 17 (Th17) cells. In a murine model of LPS-induced septic shock, treatment with NFP1 or NFP2 significantly improved survival, reduced clinical severity, and mitigated tissue damage in vital organs. These findings identify a new mechanism regulating Arid5a activity and present Arid5a allosteric inhibition as a promising therapeutic strategy for managing systemic inflammation including sepsis.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptide exchange-competent class I MHC molecules produced in eukaryotic cells for rapid production of MHC multimers.","authors":"Vasanthi Ramachandiran, John C Shires, Richard A Willis, Ge Bai, Donielle L Bell, Lixia Han, Tamara R Kazarian, Fred O Ede, Oskar Laur, Sujin Lee, Dale L Long, John D Altman","doi":"10.1093/jimmun/vkag210","DOIUrl":"10.1093/jimmun/vkag210","url":null,"abstract":"<p><p>Class I MHC peptide (MHC-Ip) multimers are well-established reagents that detect antigen-specific T cells. The classical method for production of MHC-Ip multimers begins with the expression of MHC heavy chains (HCs) and β2-microglobulin (β2m) subunits as inclusion bodies in Escherichia coli and is followed by denaturant solubilization, in vitro folding in the presence of a defined peptide ligand, and purification by size exclusion chromatography. This protocol is labor intensive, difficult to scale, and represents a significant bottleneck in application of the technology. Herein, we present a novel method for the expression in eukaryotic cells of secreted peptide exchange-competent class I MHC proteins in their native conformation. In this method, expression constructs are engineered as bimolecular complexes composed of an MHC HC and a β2m molecule covalently linked at its amino terminus to an MHC-binding peptide through a flexible peptide linker containing a defined protease site. Upon proteolysis, the original peptide occupant of the MHC binding site dissociates and is easily replaced with a synthetic peptide. When leucine zippers are added to the carboxyl terminus of each subunit, protease cleavage of the linker results in a stable HC/β2m complex that can be isolated and stored for subsequent peptide loading. Using this method, we have produced homogeneous MHC-Ip complexes for 25 class I MHC alleles and demonstrated that tetramers produced in this way are equivalent to conventionally produced tetramers for T-cell staining.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13433367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis.","authors":"Decheng Li, Daniel P Reay, Yang Li, Shachi P Vyas, Kenta Yamamoto, Dana P Ascherman, Sarah L Gaffen","doi":"10.1093/jimmun/vkag225","DOIUrl":"10.1093/jimmun/vkag225","url":null,"abstract":"<p><p>Idiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease targeting muscle and extramuscular organs, but the molecular mechanisms driving IIM pathogenesis remain largely undefined. Muscle fibroblasts are central to orchestrating inflammation in myositis. Here, we investigated muscle fibroblast dynamics using a single-cell RNA sequencing approach in an established murine model of anti-histidyl-tRNA synthetase (HRS, also known as Jo-1)-induced myositis. In fibroblasts, there was a robust activation of an IL-17 gene signature during disease. Among the induced genes was Nfkbiz, which encodes IκBζ, a noncanonical NF-κB transcriptional coactivator known to be key for pathologic IL-17 signaling in a variety of autoimmune settings. In muscle fibroblasts, IκBζ was potently activated by IL-17 in vitro and was essential for IL-17 signaling responsiveness. Surprisingly, however, the IL-17-IκBζ signaling axis was dispensable for the histopathological phenotype in HRS-induced myositis. Thus, despite a prominent IL-17 transcriptional signature, IL-17 and IκBζ are not required for autoantibody production or tissue inflammation in this model system.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13439884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sorting nexin 5 deficiency impairs MHC class II antigen presentation and inflammatory responses during tuberculosis.","authors":"Beatriz R S Dias, Kubra F Naqvi, Victoria A Ektnitphong, Samuel Alvarez-Arguedas, Kathryn C Rahlwes, Priscila C Campos, Michael U Shiloh","doi":"10.1093/jimmun/vkag217","DOIUrl":"10.1093/jimmun/vkag217","url":null,"abstract":"<p><p>Tuberculosis (TB) remains one of the leading causes of death from a single infectious agent worldwide, yet the host pathways that regulate antigen presentation and lung inflammation during Mycobacterium tuberculosis (Mtb) infection are incompletely defined. Sorting nexin 5 (SNX5) is a protein implicated in endosomal trafficking, antigen processing, and antiviral host defense, but its contribution to antibacterial immunity is unknown. Here, we show that SNX5-deficient mice exhibit increased mortality following low-dose aerosol Mtb infection despite unchanged pulmonary bacterial burden compared with wild-type mice. Snx5-/- mice developed exacerbated lung inflammation without major alterations in immune cell recruitment. In macrophages, Snx5 did not affect phagocytosis, vacuolar maturation, intracellular bacterial control, or global transcriptional responses to Mtb but was required for efficient major histocompatibility complex (MHC) class II antigen presentation. Snx5 deficiency was associated with reduced endolysosomal proteolysis and impaired MHC class II antigen presentation in vitro, resulting in reduced activation of antigen-specific CD4+ T cells without altering surface MHC class II abundance or costimulatory molecule expression. Together, these findings identify SNX5 as a regulator of MHC class II antigen presentation that influences inflammatory outcomes during pulmonary Mtb infection.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13450273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148689247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elastase and myeloperoxidase participate in neutrophil extracellular trap release stimulated by SARS-CoV-2.","authors":"Juliana da Costa Silva, Cícero Almeida, Bruna M Souza Silva, Beatriz de S Bonfim, Ayda H Schneider, Anderson Dos Santos Ramos, Isadora Marques Paiva, Letícia S Galant, Ronaldo Martins, Daniel Macedo de Melo Jorge, Victor Ferreira Costa, Guilherme C Martelossi Cebinelli, Juliana E Toller-Kawahisa, Giovanni F Gomes, Gabriel Victor Lucena da Silva, Robertha M R Lemes, Gabriel Azevedo Publio, Fernanda M de Souza, Paulo Sérgio de A Augusto, Eurico Arruda, Paulo Louzada-Junior, Pérsio da Costa Roxo-Júnior, Larissa Cunha, Letícia Bonjorno, Renê de Oliveira, Ana Paula Carlotti, Thiago Mattar Cunha, José Carlos Alves-Filho, Fernando Queiroz Cunha","doi":"10.1093/jimmun/vkaf313","DOIUrl":"10.1093/jimmun/vkaf313","url":null,"abstract":"<p><p>COVID-19 is a disease triggered by SARS-CoV-2 and some individuals develop a severe form that can progress to multiple organ failure. Neutrophils have been described as responsible for the release of neutrophil extracellular traps (NETs). The role of the elastase and myeloperoxidase (MPO) in NET release by neutrophils stimulated by SARS-CoV-2 infection was not addressed, and it was the aim of the present study. The NET release by human neutrophils infected with SARS-CoV-2 depends on elastase/MPO migration to the nucleus. Moreover, elastase/MPO migration is a consequence of PKC and PI3K kinase activation, leading to reactive oxygen species generation by the neutrophil mitochondria and NOX-2. We also reanalyzed the single-cell RNA sequencing data available in a database and demonstrated that neutrophils from bronchoalveolar lavage (BAL) fluid of patients with COVID-19 present increased expression of genes involved in the formation of the NOX2 complex, PKC delta and members of the PI3K family. In summary, the release of NETs by neutrophils in response to SARS-CoV-2 infection depends on the sequential activation of the PKC/PI3K/ROS pathway, inducing elastase/MPO migration to the nucleus triggering the NET formation. Thus, our study demonstrates new insights into the signaling pathways that induce NETs in response to SARS-CoV-2, highlighting new targets for studies and therapies for COVID-19.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of an Fgd5-positive subset of iNKT1 cells with enhanced cytotoxicity.","authors":"Alyssa H Cull, James Lok Chi Che, Sandy MacDonald, Maria Jassinskaja, Alexander Hogg, Monika Gonka, John Davey, Ellie Bennett, Samuel Elberfeld, Grace Vasey, Miriam Belmonte, Caroline A Oedekoven, Daniel Bode, Lauren B Colborn, Cera Mai, Mika Zwart, Joanna Greenman, Emma Dann, Chenqu Suo, Nathan G F Leborgne, Dave Boucher, Sarah Teichmann, Cristina Lo Celso, Elisa Laurenti, James P Hewitson, David G Kent, Jillian L Barlow","doi":"10.1093/jimmun/vkag199","DOIUrl":"https://doi.org/10.1093/jimmun/vkag199","url":null,"abstract":"<p><p>Invariant natural killer T (iNKT) cells are unconventional ɑβ T cells that respond to lipid-based antigens. They play a vital role in response to infections and are involved in diseases such as allergic asthma and cancer. Despite clear immunological roles across multiple diseases, remarkably few tools exist to study iNKTs in vivo. In this study, we report that the Fgd5ZsGreen/+ reporter mouse widely used to study hematopoietic stem cells (HSCs) can dually serve to identify rare immune cell populations, including a subset of iNKTs. Specifically, we show that a \"non-HSC\" population of CD45+Fgd5ZsGreen+ cells reside in multiple organs including the lungs, liver, spleen, and thymus. The majority of these Fgd5ZsGreen+ cells do not express canonical HSC markers but instead express CD5. RNA sequencing of CD5+EPCR-Fgd5ZsGreen+ bone marrow cells showed greatest similarity to iNKT cells, and these findings were corroborated by additional cell surface marker analysis of TCRβint CD1d-PBS57+ iNKT cells in reporter mouse tissues. We found that roughly 20% of total thymic iNKT cells were Fgd5-ZsGreen+ and that these cells predominantly coexpressed NK1.1 and CD122, consistent with an iNKT1 cell phenotype. Transcriptomic and proteomic profiling of sorted Fgd5-ZsGreen- and Fgd5-ZsGreen+ iNKT cells revealed a number of key genes involved in cytotoxic responses as distinct between the two iNKT cell populations. These different cytotoxic profiles were further supported by cytokine expression following stimulation, indicating the potential existence of disparate iNKT1 subsets. Together, these data implicate Fgd5 expression as a powerful new tool for phenotyping and tracking cytotoxic iNKT1 cell subsets in vivo.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148808561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: p38 signaling enhances short-lived effector cell differentiation and weakens central memory CD8+ T-cell formation.","authors":"","doi":"10.1093/jimmun/vkag221","DOIUrl":"https://doi.org/10.1093/jimmun/vkag221","url":null,"abstract":"","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712744","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-L1 restrains T-cell immunity in Nile tilapia by suppressing activation-induced fatty acid synthesis.","authors":"Jiansong Zhang, Kunming Li, Yuqing Yang, Shiqi Tang, Kang Li, Jialong Yang, Xiumei Wei","doi":"10.1093/jimmun/vkag236","DOIUrl":"https://doi.org/10.1093/jimmun/vkag236","url":null,"abstract":"<p><p>The programmed death ligand 1/programmed cell death 1 (PD-L1/PD-1) serves as a critical immune checkpoint in T cell-mediated immune responses, playing a central role in maintaining peripheral immune tolerance and homeostasis. Although early vertebrates lack a PD-1 homolog and they retain PD-L1, the functional significance and regulatory mechanisms of PD-L1 in T-cell immunity in these species remain poorly understood. In this study, using Nile tilapia (Oreochromis niloticus) as a teleost model, we systematically investigated the immunosuppressive role of PD-L1 in T-cell immunity. PD-L1 was widely expressed in various lymphoid tissues, and both its mRNA and protein levels were significantly upregulated following T-cell activation induced by mAbs against CD3/CD28 and Edwardsiella piscicida infection. Functional analyses demonstrated that exogenous PD-L1 treatment markedly suppressed T-cell activation and promoted activation-induced apoptosis. Moreover, PD-L1 treatment significantly impaired T-cell proliferation, effector cytokine production, and cytotoxic activity, ultimately compromising antibacterial immune defense. Mechanistically, activated tilapia T cells exhibited enhanced de novo fatty acid synthesis, whereas PD-L1 disrupted this metabolic reprogramming by inhibiting key enzymatic activities and reducing acetyl-CoA accumulation, ultimately leading to impaired T-cell function. Notably, restoration of fatty acid synthesis effectively reversed the PD-L1-induced immunosuppressive effects on tilapia T cells. In summary, this study reveals a previously unrecognized mechanism by which PD-L1 suppresses T-cell immunity in an early vertebrate through modulation of lipid metabolism. These findings highlight the essential role of metabolism regulation in immune checkpoint signaling and provide new evolutionary insights into the maintenance of T-cell homeostasis.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148794051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRECing down the source: naive and memory T cell generation in dirty mice and men.","authors":"Lyanne Y Derksen, Elena S de Dios Panal, Tamara M J Brouwers, Erdem Sanal, Anouk B Schuren, Liset Westera, Sara P H van den Berg, Debbie van Baarle, Rob J de Boer, Stephan P Rosshart, Kiki Tesselaar, José A M Borghans","doi":"10.1093/jimmun/vkag216","DOIUrl":"https://doi.org/10.1093/jimmun/vkag216","url":null,"abstract":"<p><p>Healthy aging relies on the maintenance of a diverse T cell pool. This diversity is ensured by balancing thymic output, differentiation of naive into memory T cells, T cell proliferation and cell death. For naive T cells, the balance of these processes differs between standard laboratory mice and humans. This may be a true species difference or, alternatively, result from the vastly different amounts of antigens to which standard laboratory mice and humans are exposed. Using wildlings, that is, laboratory mice born to wild mice, we studied the impact of antigen-exposure through a natural microbiome on naive and memory T cell maintenance. We found that standard laboratory mice and wildlings maintain their naive T cell pools similarly: naive T cells rarely divide and are replaced by thymic emigrants at similar rates. The daily replacement rate of memory T cells, on the other hand, is about 50% faster in wildlings than in standard laboratory mice. In both types of mice, about 20% of newly produced memory T cells originate from recruitment of naive T cells, while the remaining cells are produced by their clonal expansion and by self-renewal. In older mice, this drops to 5%. In humans, a similarly large fraction of memory cells originate from recruitment of naive T cells. Unlike in mice, most naive T cells in human adults are formed by naive T cell proliferation. Thus, while both types of mice mimic the maintenance mechanisms of the memory T cell pool in humans, even wildlings fall short as a model for human naive T cell maintenance.</p>","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":"215 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148712727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}