Cellular &Molecular Immunology最新文献

{"title":"NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers","authors":"M. Thakur, D. Mutyala, A. A. Amoliga, M. Contin Ortega, S. Batra","doi":"10.1038/s41423-026-01447-2","DOIUrl":"10.1038/s41423-026-01447-2","url":null,"abstract":"NADPH oxidases (NOXs) have emerged as central hubs that link environmental, metabolic, and immune cues through spatially organized redox signaling. However, their roles across tissues and disease states have not been comprehensively evaluated in an integrated manner. This review integrates recent advances in structural biology, immunometabolism, toxicology, and systems biology to provide an updated, comprehensive, and accessible view of NOX biology. Recent advances in high‑resolution cryo-EM, AlphaFold‑based modeling and molecular dynamics studies have provided new insights into NOX architecture, catalytic sites, post‑translational modifications and regulatory mechanisms, and docking interfaces for RAC1 and p47phox. Emerging evidence further indicates that cellular NOX-derived ROS can reprogram macrophage and T-cell metabolism, stabilize HIF-1α, and tune the balance between effector and regulatory states, thereby linking NOX activity to checkpoint control and tumor immune escape. A second focus is on how real‑world pollutants converge on NOX isoforms as proximal mediators of redox signaling across lung, vascular, hepatic, renal, and neural tissues. NOX activation during cellular injury may contribute to oxidative stress, mitochondrial dysfunction, inflammasome activation, and fibrotic signaling, through extracellular vesicles, lipid rafts, and noncoding RNAs. Finally, the review evaluates emerging therapeutic strategies, including isoform-selective/pan-NOX/peptide inhibitors, and nanozymes. It also discusses emerging approaches such as exosome-based biomarkers, network pharmacology, and machine learning for patient stratification and pharmacodynamic monitoring. By highlighting key mechanistic gaps and translational opportunities, this review establishes NOXs as actionable nodal regulators at the intersection of immunity, metabolism, environmental exposure, and human disease.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 9","pages":"1055-1109"},"PeriodicalIF":23.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41423-026-01447-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148812180","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":"Metabolic switch: lymphocytes and the onset of T-cell-mediated autoimmunity","authors":"Andisheh Mosaffa Jahromi, Fatemeh Mirzaei, Sara Mirzazadeh, Seppo Meri, Dieter Kabelitz, Kurosh Kalantar","doi":"10.1038/s41423-026-01460-5","DOIUrl":"10.1038/s41423-026-01460-5","url":null,"abstract":"T cell-mediated autoimmune diseases, including multiple sclerosis (MS), rheumatoid arthritis (RA), and type 1 diabetes (T1D), are being increasingly recognized as disorders driven not only by immune dysregulation but also by profound metabolic reprogramming in lymphocytes. Emerging evidence from the field of immunometabolism reveals that altering the balance between oxidative phosphorylation (OXPHOS) and aerobic glycolysis, along with enhancing fatty acid synthesis and dysregulated glutamine metabolism, critically shapes lymphocyte activation, differentiation, and pathogenicity. Here, we review the metabolic pathways that regulate T cells and B cells. We discuss how changes in glucose, lipid, and mitochondrial metabolism influence immune responses that lead to chronic inflammation and autoimmunity in MS, RA, and T1D. Interestingly, similar immunometabolic changes, such as increased glycolysis, mitochondrial dysfunction, and mTOR signaling, have been identified in another autoimmune disorder, systemic lupus erythematosus (SLE). Connecting metabolic dysregulation to immune tolerance failure, this review highlights immunometabolism as a key mechanism in autoimmunity. Immunometabolic pathways represent a new avenue for precision immunotherapy, although challenges persist in targeting cells specifically without systemic toxicity. Understanding these metabolic adaptations and epigenetic–metabolic crosstalk will be essential for translating these insights into next-generation therapies.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1171-1193"},"PeriodicalIF":23.9,"publicationDate":"2026-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41423-026-01460-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148807868","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":"Plakophilin 1 suppresses keratinocyte innate immune responses through DExD/H helicases","authors":"René Keil, Danny Misiak, Stefan Hüttelmaier, Frederik Tellkamp, Marcus Krüger, Mechthild Hatzfeld","doi":"10.1038/s41423-026-01462-3","DOIUrl":"10.1038/s41423-026-01462-3","url":null,"abstract":"The innate immune response is a first line of defense that allows a rapid reaction to pathogens as well as molecules released from damaged cells. It relies on pathogen-sensing receptors, many of which are nucleic acid-binding proteins, including RNA helicases. Plakophilin 1 (PKP1) is a desmosomal protein essential for strong intercellular adhesion and epithelial barrier integrity. Loss-of-function mutations in PKP1 cause ectodermal dysplasia–skin fragility syndrome (EDSFS), which is characterized by skin fragility, chronic inflammation, and recurrent infections. Here, we report that PKP1, whose role in barrier formation is to function as a critical regulator of innate immune responses. PKP1 sequesters a subset of dsRNAs that sense DExD/H-box RNA helicases—DDX1, DDX3X, DDX21, and DHX15. This limits their ability to activate the MDA5-MAVS signaling axis and prevents excessive activation of IRF3- and NFκB-driven gene expression, including the synthesis of proinflammatory cytokines, mainly IFN-β1, IL6, and TNFα. The inhibitory role of PKP1 is erased during innate immune responses by dsRNA cues, inducing proteasomal PKP1 degradation. This releases sequestered helicases, enabling dsRNA sensing and a rapid inflammatory response. Collectively, these findings identify PKP1 as a key gatekeeper that prevents exaggerated inflammation in quiescent keratinocytes, which is supported by excessive inflammation in EDSFS upon PKP1 loss. In healthy keratinocytes with proinflammatory traits, PKP1 is rapidly degraded, allowing the activation of the MDA5-MAVS signaling cascade by helicases to initiate inflammation. Hence, PKP1 combines two complementary functions essential for epidermal immune homeostasis: it provides a physical barrier preventing substance entry and suppresses innate immune responses in keratinocytes.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1269-1284"},"PeriodicalIF":23.9,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41423-026-01462-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788797","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":"Blocking the m6Am methyltransferase PCIF1 in macrophages attenuates colitis progression by preventing neuronal damage","authors":"Chenbo Ding, Jiachen Zhao, Tian Zhao, Ye Xiao, Kai Li, Xiao Liu, Xuyang Ge, Demeng Qin, Zhiqian Huang, Yu Zhang, Hua Liu, Zhiqing Diao, Youqiong Ye, Richard A. Flavell, Cheng Luo, Shijie Chen, Chengqi Yi, Zhengting Wang, Hua-Bing Li","doi":"10.1038/s41423-026-01459-y","DOIUrl":"10.1038/s41423-026-01459-y","url":null,"abstract":"Macrophage–enteric neuron dialog is crucial for intestinal homeostasis, but its specific role and underlying mechanism in inflammatory bowel disease (IBD) pathogenesis remain elusive. Here, we demonstrate that colonic macrophage-mediated extracellular matrix (ECM) remodeling orchestrates enteric neuronal maturation and dictates colitis progression. The depletion of Pcif1, recognized as a unique methyltransferase for m6Am mRNA methylation, in macrophages attenuates colitis and protects enteric neurons from inflammation-driven degeneration. Specifically, Pcif1-deficient macrophages increase ECM accumulation, promoting their own extravasation into enteric neuronal plexuses and the maturation of enteric neurons, thereby curbing inflammation-driven neuronal injury and colitis progression. Mechanistically, Pcif1-mediated m6Am modification inhibits the translation of Znf219 mRNA and represses the Znf219-Egr1 axis, a master transcriptional module that governs ECM remodeling. Finally, pharmacological blockade of PCIF1 promotes macrophage-mediated ECM deposition and suppresses colitis and neuronal loss. Our findings reveal a novel mechanism whereby ECM remodeling in macrophages drives enteric neuronal maturation and illuminate the m6Am machinery as a promising therapeutic target for preventing neuronal loss in IBD patients.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1250-1268"},"PeriodicalIF":23.9,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148788826","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":"The FAM234A-USP4 axis governs T-cell fate through the dual regulation of mTOR and RORγt","authors":"Hai Wang, Deyu Fang","doi":"10.1038/s41423-026-01454-3","DOIUrl":"10.1038/s41423-026-01454-3","url":null,"abstract":"","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 9","pages":"1169-1170"},"PeriodicalIF":23.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757641","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":"Radiation-induced CD200+ tumor-associated macrophages suppress eosinophil-mediated antitumor immunity through CD200R signaling in hepatocellular carcinoma","authors":"Kun Li, Siqi Li, Dongbo Qiu, Xiusheng Qiu, Haoyuan Yu, Yi Xiong, Wei Liang, Zhixing Liang, Shuqun Cheng, Hua Li, Yunfei Qin, Yang Yang, Linsen Ye","doi":"10.1038/s41423-026-01456-1","DOIUrl":"10.1038/s41423-026-01456-1","url":null,"abstract":"Radiotherapy elicits dual immunomodulatory effects in cancer, activating antitumor immunity while paradoxically inducing immunosuppression, which limits therapeutic efficacy. The molecular pathways mediating postradiation immune escape in hepatocellular carcinoma (HCC) remain poorly defined. Here, we elucidate a previously uncharacterized mechanism whereby radiotherapy drives the accumulation of CD200+ tumor-associated macrophages (TAMs) that suppress eosinophil-mediated antitumor immunity in patients with HCC. Through single-cell RNA sequencing of postradiotherapy HCC specimens, we demonstrated that radiation-induced DNA damage activated the cytosolic DNA-sensing STING pathway in TAMs, triggering NF-κB-dependent CD200 upregulation independent of canonical type I interferon signaling. These radiation-induced CD200+ TAMs exhibited an immunosuppressive phenotype and correlated with adverse clinical outcomes in HCC patients. Mechanistically, CD200+ TAMs established an immunosuppressive axis by recruiting CCR1+ eosinophils through CCL3-mediated chemotaxis, subsequently inhibiting their antitumor functions via CD200-CD200R engagement. This interaction comprehensively suppressed NF-κB activation in eosinophils, impaired their antigen-presenting capacity and Th2 cytokine secretion and abrogated their ability to support CD8+ T-cell-mediated cytotoxicity. Therapeutic blockade of CD200R following radiotherapy restored eosinophil effector functions, promoted central memory T-cell formation, and significantly enhanced tumor control across multiple preclinical HCC models. Remarkably, CD200R antagonism sensitized PD-1-refractory “cold” tumors to radioimmunotherapy combinations, overcoming primary resistance. Our findings establish STING-driven CD200+ TAM accumulation and subsequent eosinophil dysfunction as critical determinants of radioresistance, positioning CD200R blockade as a promising therapeutic strategy to potentiate radioimmunotherapy responses in patients with HCC.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 9","pages":"1152-1168"},"PeriodicalIF":23.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757823","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":"MARCH2/3 target FcγRI for K27-linked polyubiquitination and degradation to restrict the inflammatory response","authors":"Qi Zhang, Xu Chen, Xu Zhang, Shi-Tong Lu, Jin-Xi Yu, Hong Bai, Hong-Bing Shu, Shu Li","doi":"10.1038/s41423-026-01457-0","DOIUrl":"10.1038/s41423-026-01457-0","url":null,"abstract":"IgG Fc gamma receptor I (FcγRI) belongs to the immunoglobulin superfamily and plays a pivotal role in immune regulation. The post-translational regulation of FcγRI and its effects on immune regulation are unclear. In this study, we identified the membrane-associated RING-CH-type finger (MARCH) E3 ubiquitin ligases MARCH2 and MARCH3 as physiological regulators of FcγRI. MARCH2 and MARCH3 associate with FcγRI and mediate its K27-linked polyubiquitination at K336 and K368, respectively, leading to subsequent lysosomal degradation. While deficiency of either MARCH2 or MARCH3 modestly increases FcγRI levels as well as LPS- and IgG-induced transcription of downstream genes, double knockout of MARCH2/3 has a more dramatic effect. Double knockout of MARCH2/3 increases LPS-induced transcription of downstream genes in wild-type but not FcγRI knockout cells, and reconstitution of FcγRIK336R/K368R into FcγRI-deficient cells increases LPS-induced transcription of the downstream genes to a higher degree than reconstitution with wild-type FcγRI. Individual knockout of MARCH2 or MARCH3 sensitizes mice to LPS-induced lung injury and Salmonella typhimurium-induced inflammation, and these effects are more severe in MARCH2/3 double-knockout mice. These findings suggest that MARCH2 and MARCH3 redundantly target FcγRI for K27-linked polyubiquitination and lysosomal degradation, thereby acting as host factors to limit the FcγRI-mediated inflammatory response and pathogenesis.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1235-1249"},"PeriodicalIF":23.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757916","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":"IL-17D reprograms CD93+ antigen-presenting cells in the glioblastoma microenvironment","authors":"Weijie Tang, Shuyuan Zhang, Yanhua Qi, Boyan Li, Zijie Gao, Ziwen Pan, Jiawei Qiu, Hao Xue, Gang Li, Shaobo Wang","doi":"10.1038/s41423-026-01458-z","DOIUrl":"10.1038/s41423-026-01458-z","url":null,"abstract":"The immunosuppressive microenvironment is a hallmark of glioblastoma (GBM), limiting the efficacy of contemporary immunotherapies. While the central nervous system (CNS) relies on specialized cytokine networks to maintain immune homeostasis under physiological conditions, how these homeostatic signals are subverted during gliomagenesis remains poorly understood. Here, we report that interleukin-17D (IL-17D) is a CNS-intrinsic tumor suppressor whose expression is downregulated during gliomagenesis. Restoring IL-17D substantially extends survival in orthotopic GBM models by selectively reprogramming the myeloid compartment. Mechanistically, IL-17D engages its receptor CD93 to assemble a novel costimulatory receptor complex with SCARB1 in a lipid raft-dependent manner. This structural assembly engages Fyn/BCAP to trigger PI3K/AKT/NF-κB signaling, effectively inverting the function of SCARB1 from tolerogenic efferocytosis to active antigen presentation. Our study demonstrated that the restoration of IL-17D expression reshaped the GBM immune landscape, highlighting its potential as a therapeutic target to enhance the efficacy of immunotherapy.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1219-1234"},"PeriodicalIF":23.9,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148766447","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":"Platelet-derived serotonin epigenetically programs macrophage alternative activation to orchestrate type 2 airway inflammation","authors":"Ru Tang, Guofang Xia, Ying Zhu, Jinhong Shen, Zhihan Liu, Song Mao, Jiayao Zhou, Yuelong Gu, Shilei Pu, Zhipeng Li, Hai Lin, Congfeng Xu, Hongqing Xu, Feng Zhang, Yongxu Zhao, Shankai Yin, Weitian Zhang, Feng Liu","doi":"10.1038/s41423-026-01455-2","DOIUrl":"10.1038/s41423-026-01455-2","url":null,"abstract":"Type 2 inflammation (T2I) drives chronic airway diseases such as eosinophilic chronic rhinosinusitis (eCRS) and asthma, which are frequently accompanied by coagulation activation and platelet recruitment. However, whether and how these associated processes actively contribute to shaping inflammation remain largely unknown. Here, using single-cell transcriptomic profiling of human nasal polyp samples from eCRS patients with or without comorbid asthma, we identified a TGM2hi macrophage population enriched in inflamed tissues and strongly correlated with local eosinophilia and systemic disease burden. Using dust mite-induced type 2 airway inflammation models in mice, we showed that the loss of Tgm2, either globally or in macrophages, selectively impaired alternative macrophage activation and attenuated both eosinophilic inflammation and epithelial remodeling. Mechanistically, TGM2 catalyzes the recently described histone modification H3Q5 serotonylation (H3Q5Ser), promoting an epigenetically permissive chromatin state for alternative macrophage activation. We further revealed a transcellular circuit driven by the activated platelet-derived monoamine metabolite serotonin (5-HT), which acts as a critical paracrine signal to fuel this epigenetic reprogramming of macrophages. Crucially, pharmacological inhibition of platelet 5-HT release or TGM2 activity ameliorated both nasal and pulmonary pathology in a mouse model of type 2 inflammation, underscoring the therapeutic potential of this pathway. Our findings establish a serotonin-TGM2-H3Q5Ser axis that couples platelet activation to macrophage epigenetic programming. This transcellular mechanism drives type 2 inflammation and reveals novel therapeutic opportunities across airway diseases.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 10","pages":"1368-1386"},"PeriodicalIF":23.9,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41423-026-01455-2.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629646","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":"NLRC3 enhances antitumor immunity by specifically negatively regulating M-MDSCs in a STING-dependent manner","authors":"Yuling Fu, Xiaoxia Zhan, Shousheng Liu, Qinhan Xie, Shijie Song, Suwan Wu, Junli Sheng, Huiru He, Xiaolong You, Qiao Ling, Xiaodan Yang, Zulaya Abudureyimu, Wenhao Lu, Wen Li, Jia Tang, Peng Wang, Shengfeng Hu","doi":"10.1038/s41423-026-01453-4","DOIUrl":"10.1038/s41423-026-01453-4","url":null,"abstract":"NOD-like receptor (NLR) family CARD domain containing 3 (NLRC3), an intracellular member of the NLR family, is a negative regulator of both immune cell modulation and tumor cell proliferation. However, the role of NLRC3 and the mechanisms underlying its effect on the tumor immune microenvironment remain unclear. In this study, we report that NLRC3 promotes antitumor immunity by specifically negatively regulating the infiltration and immunosuppressive function of monocytic myeloid-derived suppressor cells (M-MDSCs). Mechanistically, NLRC3 inhibits the stimulator of interferon genes (STING) signaling pathway, leading to reduced expression of programmed cell death ligand 1 (PD-L1) and CCR2 in M-MDSCs, thereby limiting the infiltration and immunosuppressive function of M-MDSCs. Notably, overexpression of NLRC3 in combination with the STING agonist c-GAMP significantly inhibited tumor growth. These findings reveal a critical role for NLRC3 in modulating the immune microenvironment and provide insights into the optimization of NLRC3-targeted therapeutics.","PeriodicalId":9950,"journal":{"name":"Cellular &Molecular Immunology","volume":"23 9","pages":"1127-1137"},"PeriodicalIF":23.9,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618616","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}