ImmunityPub Date : 2026-09-23DOI: 10.1016/j.immuni.2026.08.013
Sergio Villazala-Merino,Lucas Bertoia,Romain Fenouil,Mohammed Zghaebi,Myriam Moussa,Samuel Origlio,Claude Gregoire,Laura Almada,Mara Esposito,Stefano A.P. Colombo,Adriana Gruppi,Judith E. Allen,Andrew S. MacDonald,Nicolas Fazilleau,Pierre Bruhns,Julia Eckl-Dorna,Carolyn G. King,Mauro Gaya
{"title":"Germinal center interleukin-4 microniches drive tissue divergence of IgE memory B cell responses","authors":"Sergio Villazala-Merino,Lucas Bertoia,Romain Fenouil,Mohammed Zghaebi,Myriam Moussa,Samuel Origlio,Claude Gregoire,Laura Almada,Mara Esposito,Stefano A.P. Colombo,Adriana Gruppi,Judith E. Allen,Andrew S. MacDonald,Nicolas Fazilleau,Pierre Bruhns,Julia Eckl-Dorna,Carolyn G. King,Mauro Gaya","doi":"10.1016/j.immuni.2026.08.013","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.08.013","url":null,"abstract":"Immunoglobulin E (IgE) drives allergy, yet how memory B cells (MBCs) reactivate to produce IgE, and how tissue localization shapes recall responses, remains unclear. Using mouse models of airborne exposure to house dust mites and Alternaria, we found that allergen sensitization generated lymph node (LN)- and lung-resident MBCs. Upon allergen re-exposure, MBCs follow two differentiation trajectories: a germinal center (GC)-dependent pathway, generating IgG1+ and IgE+ plasma cells (PCs) and occurring predominantly in LNs, and a GC-independent pathway, generating mainly IgG1+ PCs and present in both organs. GC re-entry granted MBCs access to an interleukin (IL)-4-rich microniche formed by T follicular helper (Tfh) cells, which was essential for IgE production. Disrupting GC re-entry, IL-4 signaling, or Tfh cell-derived IL-4 during recall markedly reduced allergen-specific IgE. These findings reveal a spatially and cytokine-restricted mechanism that confines IgE memory to lymphoid organs, positioning GC IL-4 microniches as anatomical safeguards against IgE production at barrier sites frequently exposed to environmental antigens.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"26 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149019708","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}
ImmunityPub Date : 2026-09-22DOI: 10.1016/j.immuni.2026.08.012
Xueping Zhu,Haibo Yang,Haoting Zhan,Isabela J. Kernin,Dean R. Buttaci,Ngoc Le,Cai Han,Parth R. Naik,Peri R. Matatia,Sarah Zaghouani,Lillian R. Delacruz,Lukas M. Altenburger,Neal P. Smith,Elena Wu,Rebecca Londoner,Cameron H. Flayer,Zhengwang Sun,Alison E. Ringel,Alexandra-Chloe Villani,Rod A. Rahimi,Caroline L. Sokol
{"title":"Sensory neuronal mTORC1 kinase signaling establishes neuroimmune memory that initiates allergic immunity","authors":"Xueping Zhu,Haibo Yang,Haoting Zhan,Isabela J. Kernin,Dean R. Buttaci,Ngoc Le,Cai Han,Parth R. Naik,Peri R. Matatia,Sarah Zaghouani,Lillian R. Delacruz,Lukas M. Altenburger,Neal P. Smith,Elena Wu,Rebecca Londoner,Cameron H. Flayer,Zhengwang Sun,Alison E. Ringel,Alexandra-Chloe Villani,Rod A. Rahimi,Caroline L. Sokol","doi":"10.1016/j.immuni.2026.08.012","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.08.012","url":null,"abstract":"Environmental allergens are enriched in protease activity, which activates cutaneous sensory neurons, triggering itch and substance P release to promote migration of T helper (Th)2 cell-skewing CD301b+ dendritic cells and initiate allergic immunity. However, allergens are typically encountered through repeated subthreshold exposures, and how these cumulatively induce sensitization is unknown. We identified a sensory neuron-intrinsic mechanism of neuroimmune memory. Protease allergen exposure induced sustained mechanistic target of rapamycin complex 1 (mTORC1) kinase signaling and transcriptional activator peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α)-associated mitochondrial remodeling in sensory neurons, establishing a metabolically primed state with enhanced neuronal responsiveness. Upon allergen re-exposure, this state drove enhanced itch, CD301b+ dendritic cell migration, and Th2 cell differentiation. Disrupting neuronal mTORC1 signaling or mitochondrial stability abrogated this amplification while sparing primary responses. This mechanism generalized across distinct protease allergens, revealing mTORC1-driven metabolic reprogramming in sensory neurons as a form of innate neuroimmune memory underlying allergen cross-sensitization and polysensitization.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"47 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149013592","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}
ImmunityPub Date : 2026-09-17DOI: 10.1016/j.immuni.2026.08.011
Koji Haratani,Bruce Reinhold,Jonathan S. Duke-Cohan,Caroline G. Fahey,Kemin Tan,Robert J. Mallis,Alexander Gusev,Kenneth L. Kehl,Jia Luo,Allyson Karmazyn,Elizabeth L. Holliday,Daniel J. Masi,Katarzyna J. Zienkiewicz,Connor J. Hennessey,Rafael B. Blasco,Tran C. Thai,Grace M. Gibbons,Sophie Kivlehan,Patrick Lizotte,Cloud P. Paweletz,Andrew J. Aguirre,Keith L. Ligon,Roberto Chiarle,Matthew J. Lang,David A. Barbie,Ellis L. Reinherz
{"title":"Cancers modulate processing and presentation of p53 neoantigens to evade T cell detection","authors":"Koji Haratani,Bruce Reinhold,Jonathan S. Duke-Cohan,Caroline G. Fahey,Kemin Tan,Robert J. Mallis,Alexander Gusev,Kenneth L. Kehl,Jia Luo,Allyson Karmazyn,Elizabeth L. Holliday,Daniel J. Masi,Katarzyna J. Zienkiewicz,Connor J. Hennessey,Rafael B. Blasco,Tran C. Thai,Grace M. Gibbons,Sophie Kivlehan,Patrick Lizotte,Cloud P. Paweletz,Andrew J. Aguirre,Keith L. Ligon,Roberto Chiarle,Matthew J. Lang,David A. Barbie,Ellis L. Reinherz","doi":"10.1016/j.immuni.2026.08.011","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.08.011","url":null,"abstract":"TP53 mutations occur early in malignant transformation as truncal events in tumor evolution and are therefore generally present in all descendant tumor cells, creating an immunological vulnerability. Here, we examined the immunogenicity and antigenicity of p53 neoantigens emerging from these truncal mutations. Comprehensive immunopeptidomics revealed that hotspot mutations in human tumors preferentially localize to p53 regions resistant to antigen processing, thereby avoiding display altogether. Moreover, for neoantigens presentable by HLA-A∗02:01 or HLA-B∗07:02 and structurally divergent from corresponding wild-type p53 peptide-HLA complexes, clinical tumors commonly lacked the relevant presenting HLA allele. Tumor cells further resisted T cell killing through increased activity of the aminopeptidase ERAP1, preventing display of high-affinity HLA-A∗02:01 complexes containing an immunogenic p53I195F-derived 11-mer, or by expressing low-affinity HLA-A∗02:01 complexes containing a p53R175H-derived 9-mer with poor antigenicity despite high-quality human TCRs. These findings define mechanisms by which tumors restrict targetable truncal neoantigen display and suggest immunopeptidome shift strategies to circumvent immune escape.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"61 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148980650","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}
ImmunityPub Date : 2026-09-08DOI: 10.1016/j.immuni.2026.08.008
Joanne E. Konkel,Sarah L. Gaffen
{"title":"Speedy delivery: EV-derived fungal antigens establish oral-gut Th17 crosstalk","authors":"Joanne E. Konkel,Sarah L. Gaffen","doi":"10.1016/j.immuni.2026.08.008","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.08.008","url":null,"abstract":"Candida albicans induces Th17 cells, but their origins remain unresolved. In this issue of Immunity, Martini et al. show that the mouth is a reservoir for fungal Th17 cells that adopt pathogenic signatures in the gut during Crohn’s disease.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"376 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148902463","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}
ImmunityPub Date : 2026-09-08Epub Date: 2026-07-14DOI: 10.1016/j.immuni.2026.06.013
Gabriela Rios Martini, Philipp Hofmann, Ann-Kristin Kamps, Amos Weichberger, Ekaterina Tikhonova, Aidan Conroy, Xiangyu Pan, Diana Milagros Namuch, Laura Rathjens, Arne Bergfeld, Susanna Nikolaus, Jeanette Riffert, Florian Tran, Konrad Aden, Maria Witte, Clemens Schafmayer, Dora Stölzl, Stephan Weidinger, Markus M Heimesaat, Miriam Cyris, Ann-Kristin Härdter, Christof Dörfer, Robert Zarnowski, David Andes, Sascha Brunke, Bernhard Hube, Alexander Scheffold, Iliyan D Iliev, Stefan Schreiber, Petra Bacher
{"title":"Antigen-restricted Candida albicans Th17 cells link oral-gut immunity and adopt pathogenic features during intestinal inflammation.","authors":"Gabriela Rios Martini, Philipp Hofmann, Ann-Kristin Kamps, Amos Weichberger, Ekaterina Tikhonova, Aidan Conroy, Xiangyu Pan, Diana Milagros Namuch, Laura Rathjens, Arne Bergfeld, Susanna Nikolaus, Jeanette Riffert, Florian Tran, Konrad Aden, Maria Witte, Clemens Schafmayer, Dora Stölzl, Stephan Weidinger, Markus M Heimesaat, Miriam Cyris, Ann-Kristin Härdter, Christof Dörfer, Robert Zarnowski, David Andes, Sascha Brunke, Bernhard Hube, Alexander Scheffold, Iliyan D Iliev, Stefan Schreiber, Petra Bacher","doi":"10.1016/j.immuni.2026.06.013","DOIUrl":"10.1016/j.immuni.2026.06.013","url":null,"abstract":"<p><p>The commensal yeast Candida albicans is a major inducer of human mucosal Th17 cells. How C. albicans drives Th17 cell responses at homeostasis, and whether such responses contribute to inflammatory diseases, remains poorly understood. Here, we showed that C. albicans-reactive Th17 cells targeted a limited set of proteins enriched in fungal extracellular vesicles. At homeostasis, these cells predominantly resided in the oral mucosa. However, T cell receptor profiling revealed shared clonotypes across oral and gut tissues, with C. albicans being a major driver of this repertoire overlap. In patients with Crohn's disease, C. albicans-specific Th17 cells with features of oral priming were enriched in intestinal tissues, where they retained their focused antigen specificity but acquired pathogenic Th17 cell traits. Together, our results reveal a stable, antigen-restricted C. albicans Th17 subset that is shared across mucosal sites and undergoes functional adaptation in the inflamed intestine. These cells represent a potential target for immune modulation in Crohn's disease.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":" ","pages":"2545-2561.e10"},"PeriodicalIF":30.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445982","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}
ImmunityPub Date : 2026-09-08DOI: 10.1016/j.immuni.2026.08.005
Bingpeng Yao,Xin Sun
{"title":"Lending an ear to the lung","authors":"Bingpeng Yao,Xin Sun","doi":"10.1016/j.immuni.2026.08.005","DOIUrl":"https://doi.org/10.1016/j.immuni.2026.08.005","url":null,"abstract":"The unprecedented recent advancement in the field of interoception (sensing self) has introduced neuromodulation as a realistic treatment approach. Shibuya et al. identified an ear-to-lung reflex in which activation of auricular-innervating TRPV1+ vagal sensory neurons functions through neuropeptide CGRPβ to suppress allergic airway inflammation, providing an elegant example of exteroceptive control of interoception and a mechanism for transcutaneous neuromodulation.","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"35 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148902465","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}
ImmunityPub Date : 2026-09-08Epub Date: 2026-07-17DOI: 10.1016/j.immuni.2026.06.020
Kathryn A Jacobs, Yichao Hua, Apostolos Panagiotis Nikolakopoulos, Swati Gupta, Gerlanda Vella, Ana Filipa Domingues Laranjeiro, Julie Bonnereau, Mélanie Guyot, Maria Livia Sassano, Larissa Mourao, Feyza Cansiz, Gabriele Allies, Nicolas Van Baren, Sophie Lucas, Hiroto Kawashima, Wiebke Sondermann, Florian Rambow, Alpaslan Tasdogan, Colinda Scheele, Patrizia Agostinis, Gabriele Bergers
{"title":"Autophagy maintains high endothelial venule identity and function during inflammation.","authors":"Kathryn A Jacobs, Yichao Hua, Apostolos Panagiotis Nikolakopoulos, Swati Gupta, Gerlanda Vella, Ana Filipa Domingues Laranjeiro, Julie Bonnereau, Mélanie Guyot, Maria Livia Sassano, Larissa Mourao, Feyza Cansiz, Gabriele Allies, Nicolas Van Baren, Sophie Lucas, Hiroto Kawashima, Wiebke Sondermann, Florian Rambow, Alpaslan Tasdogan, Colinda Scheele, Patrizia Agostinis, Gabriele Bergers","doi":"10.1016/j.immuni.2026.06.020","DOIUrl":"10.1016/j.immuni.2026.06.020","url":null,"abstract":"<p><p>High endothelial venules (HEVs) play a crucial role in adaptive immune responses in secondary lymphoid organs (SLOs). They are equipped with high amounts of peripheral node addressin (PNAd), harboring carbohydrate structures that serve as L-selectin ligands to efficiently facilitate lymphocyte homing. During inflammation, the HEV network expands in SLOs, increasing lymphocyte infiltration, but the underlying mechanisms that maintain HEVs remain underexplored. Here, we report that autophagy is essential for HEV function and expansion. Using single-cell transcriptomics, unbiased proteomics, intravital imaging, and an inducible HEV tracer system in mice, we demonstrate that autophagy deficiency compromises lymphotoxin beta receptor (LTβR) signaling and the unfolded protein response in HEVs, leading to disrupted PNAd production, dedifferentiation, and reduced lymphocyte homing. Autophagy deficiency and LTβR blockade impair HEV function and reduce skin inflammation in psoriasis-affected mice by limiting immune infiltration and cytokine release. Our work reveals that autophagy safeguards HEV identity and function during inflammation.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":" ","pages":"2429-2446.e8"},"PeriodicalIF":30.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470055","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}
ImmunityPub Date : 2026-09-08Epub Date: 2026-07-15DOI: 10.1016/j.immuni.2026.06.005
Rintaro Shibuya, Nobuya Abe, Keaton Song, Nathan D Rossen, Masato Tamari, Zhen Wang, Zili Xie, Yuki Abe, Hisato Iriki, Ayana Iijima, Lydia Zamidar, Xu Li, Xia Meng, Andras Bimbo-Szuhai, Veronica Burstein, Jill K Gregory, Natalia P Biscola, Karen Anthony, Michel Enamorado, Steven J Van Dyken, Kenji Kabashima, Hongzhen Hu, Brian S Kim
{"title":"Activation of the auricular vagus nerve reflex suppresses airway inflammation.","authors":"Rintaro Shibuya, Nobuya Abe, Keaton Song, Nathan D Rossen, Masato Tamari, Zhen Wang, Zili Xie, Yuki Abe, Hisato Iriki, Ayana Iijima, Lydia Zamidar, Xu Li, Xia Meng, Andras Bimbo-Szuhai, Veronica Burstein, Jill K Gregory, Natalia P Biscola, Karen Anthony, Michel Enamorado, Steven J Van Dyken, Kenji Kabashima, Hongzhen Hu, Brian S Kim","doi":"10.1016/j.immuni.2026.06.005","DOIUrl":"10.1016/j.immuni.2026.06.005","url":null,"abstract":"<p><p>The vagus nerve regulates inflammation via sensory-motor arcs. While vagal sensory neurons relay signals from within the body (interoception), whether external inputs can regulate visceral neuroimmune responses (exteroception) remains poorly understood. We unveiled a skin-lung reflex by which sensory neurons from the auricular skin suppressed Alternaria alternata-induced allergic airway inflammation. Viral and chemical neural tracing revealed distinct sensory projections from the vagal ganglia to the auricular skin. Pharmacologic, chemogenetic, and optogenetic activation of auricular transient receptor potential vanilloid 1 (TRPV1)<sup>+</sup> afferents attenuated type 2 allergic lung inflammation, including group 2 innate lymphoid cell, eosinophil, and type 2 cytokine responses in the airway. Conversely, silencing of these sensory neurons via the skin exacerbated lung inflammation, and immunosuppression of airway inflammation was dependent on the neuropeptide calcitonin gene-related peptide (CGRP)β. These findings reveal an evolutionarily conserved somato-visceral reflex by which exteroceptive inputs impact visceral inflammation. Thus, transcutaneous neuromodulation may represent a therapeutic strategy to treat visceral inflammation.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":" ","pages":"2402-2412.e6"},"PeriodicalIF":30.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455706","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":"Flavin adenine dinucleotide is an endogenous suppressor for cytosolic DNA and RNA sensors to modulate innate immunity.","authors":"Yao Wang, Yanyan Shen, Jiayu Liu, Qi Qi, Yue Guo, Yunying Wang, Boyang Xie, Chunyan Yan, Yanhong Liu, Zhi Jin, Ruibo Wang, Aiping Cao, Juncheng Li, Zengqing Song, Jing Chen, Qiuying Han, Yingjie Zhu, Kun Zhang, Taixia Wang, Tao Li, Xin Pan, Xinhua He, Tao Zhou, Ailing Li, Xuemin Zhang, Na Wang, Qing Xia, Weina Zhang","doi":"10.1016/j.immuni.2026.06.010","DOIUrl":"10.1016/j.immuni.2026.06.010","url":null,"abstract":"<p><p>Cytosolic DNA and RNA sensing is crucial for innate immunity, playing essential roles in pathogen defense and autoinflammation induction. We reported the endogenous metabolite flavin adenine dinucleotide (FAD) as a molecular brake restraining both cytosolic DNA and RNA sensing. It bound directly to cytosolic nucleic acid sensors cyclic GMP-AMP synthase (cGAS) and retinoic acid-inducible gene I (RIG-I), occupying catalytic pockets to suppress their activity and downstream immune responses. Physiologically, FAD prevented self-nucleic acid-induced sterile inflammation and maintained immune homeostasis. FAD deficiency due to FAD synthase (FLAD1) ablation exacerbated auto-inflammation and cellular senescence. Upon viral infection, reduced FLAD1 activity lowered FAD amounts, which removed its inhibitory control over DNA and RNA sensors, thus facilitating extensive interferon-I (IFN-I) signaling activation. Consequently, FLAD1 depletion strengthened the innate immune response and protected mice from viral infection. Our findings identify FAD as a natural suppressor of both cytosolic DNA and RNA sensing, offering therapeutic potential for inflammatory diseases.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":" ","pages":"2413-2428.e9"},"PeriodicalIF":30.6,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148436490","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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