ImmunityPub Date : 2024-07-09DOI: 10.1016/j.immuni.2024.06.007
Guilhem Pupier, Catherine Sautès-Fridman
{"title":"B cells! Don’t go the wrong way in this tumor","authors":"Guilhem Pupier, Catherine Sautès-Fridman","doi":"10.1016/j.immuni.2024.06.007","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.06.007","url":null,"abstract":"<p>The association of tertiary lymphoid structures (TLSs) with survival and immunotherapy response brought B cells to center stage. In a pan-cancer B cells atlas in <em>Science</em>, Ma et al. show that germinal center reaction generating anti-tumor antibody-secreting cells (ASCs) from B memory cells in mature TLSs co-exist in tumors with extra-follicular reaction generating auto-reactive ASCs from memory B cells in immature TLSs.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"20 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141561725","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 : 2024-07-09DOI: 10.1016/j.immuni.2024.06.009
Jason G. Cyster, Patrick C. Wilson
{"title":"Antibody modulation of B cell responses—Incorporating positive and negative feedback","authors":"Jason G. Cyster, Patrick C. Wilson","doi":"10.1016/j.immuni.2024.06.009","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.06.009","url":null,"abstract":"<p>Antibodies are powerful modulators of ongoing and future B cell responses. While the concept of antibody feedback has been appreciated for over a century, the topic has seen a surge in interest due to the evidence that the broadening of antibody responses to SARS-CoV-2 after a third mRNA vaccination is a consequence of antibody feedback. Moreover, the discovery that slow antigen delivery can lead to more robust humoral immunity has put a spotlight on the capacity for early antibodies to augment B cell responses. Here, we review the mechanisms whereby antibody feedback shapes B cell responses, integrating findings in humans and in mouse models. We consider the major influence of epitope masking and the diverse actions of complement and Fc receptors and provide a framework for conceptualizing the ways antigen-specific antibodies may influence B cell responses to any form of antigen, in conditions as diverse as infectious disease, autoimmunity, and cancer.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"34 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141561726","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 : 2024-07-03DOI: 10.1016/j.immuni.2024.06.005
Samuel W. Kazer, Colette Matysiak Match, Erica M. Langan, Marie-Angèle Messou, Thomas J. LaSalle, Elise O’Leary, Jessica Marbourg, Katherine Naughton, Ulrich H. von Andrian, Jose Ordovas-Montanes
{"title":"Primary nasal influenza infection rewires tissue-scale memory response dynamics","authors":"Samuel W. Kazer, Colette Matysiak Match, Erica M. Langan, Marie-Angèle Messou, Thomas J. LaSalle, Elise O’Leary, Jessica Marbourg, Katherine Naughton, Ulrich H. von Andrian, Jose Ordovas-Montanes","doi":"10.1016/j.immuni.2024.06.005","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.06.005","url":null,"abstract":"<p>The nasal mucosa is often the initial site of respiratory viral infection, replication, and transmission. Understanding how infection shapes tissue-scale primary and memory responses is critical for designing mucosal therapeutics and vaccines. We generated a single-cell RNA-sequencing atlas of the murine nasal mucosa, sampling three regions during primary influenza infection and rechallenge. Compositional analysis revealed restricted infection to the respiratory mucosa with stepwise changes in immune and epithelial cell subsets and states. We identified and characterized a rare subset of Krt13+ nasal immune-interacting floor epithelial (KNIIFE) cells, which concurrently increased with tissue-resident memory T (T<sub>RM</sub>)-like cells. Proportionality analysis, cell-cell communication inference, and microscopy underscored the CXCL16-CXCR6 axis between KNIIFE and T<sub>RM</sub> cells. Secondary influenza challenge induced accelerated and coordinated myeloid and lymphoid responses without epithelial proliferation. Together, this atlas serves as a reference for viral infection in the upper respiratory tract and highlights the efficacy of local coordinated memory responses.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"77 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141496051","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 : 2024-07-01DOI: 10.1016/j.immuni.2024.06.003
Munesh K. Harioudh, Joseph Perez, Lomon So, Mayank Maheshwari, Thomas S. Ebert, Veit Hornung, Ram Savan, A. Rouf Banday, Michael S. Diamond, Vijay A. Rathinam, Saumendra N. Sarkar
{"title":"The canonical antiviral protein oligoadenylate synthetase 1 elicits antibacterial functions by enhancing IRF1 translation","authors":"Munesh K. Harioudh, Joseph Perez, Lomon So, Mayank Maheshwari, Thomas S. Ebert, Veit Hornung, Ram Savan, A. Rouf Banday, Michael S. Diamond, Vijay A. Rathinam, Saumendra N. Sarkar","doi":"10.1016/j.immuni.2024.06.003","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.06.003","url":null,"abstract":"<p>An important property of the host innate immune response during microbial infection is its ability to control the expression of antimicrobial effector proteins, but how this occurs post-transcriptionally is not well defined. Here, we describe a critical antibacterial role for the classic antiviral gene 2′-5′-oligoadenylate synthetase 1 (OAS1). Human OAS1 and its mouse ortholog, Oas1b, are induced by interferon-γ and protect against cytosolic bacterial pathogens such as <em>Francisella novicida</em> and <em>Listeria monocytogenes in vitro</em> and <em>in vivo</em>. Proteomic and transcriptomic analysis showed reduced IRF1 protein expression in OAS1-deficient cells. Mechanistically, OAS1 binds and localizes IRF1 mRNA to the rough endoplasmic reticulum (ER)-Golgi endomembranes, licensing effective translation of IRF1 mRNA without affecting its transcription or decay. OAS1-dependent translation of IRF1 leads to the enhanced expression of antibacterial effectors, such as GBPs, which restrict intracellular bacteria. These findings uncover a noncanonical function of OAS1 in antibacterial innate immunity.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"80 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141489726","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 : 2024-06-21DOI: 10.1016/j.immuni.2024.05.025
Henan Xu, Xiao Zhang, Xin Wang, Bo Li, Hang Yu, Yuan Quan, Yan Jiang, Yuling You, Yan Wang, Mingyue Wen, Juan Liu, Min Wang, Bo Zhang, Yixian Li, Xuan Zhang, Qianjin Lu, Chu-Yi Yu, Xuetao Cao
{"title":"Cellular spermine targets JAK signaling to restrain cytokine-mediated autoimmunity","authors":"Henan Xu, Xiao Zhang, Xin Wang, Bo Li, Hang Yu, Yuan Quan, Yan Jiang, Yuling You, Yan Wang, Mingyue Wen, Juan Liu, Min Wang, Bo Zhang, Yixian Li, Xuan Zhang, Qianjin Lu, Chu-Yi Yu, Xuetao Cao","doi":"10.1016/j.immuni.2024.05.025","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.05.025","url":null,"abstract":"<p>Prolonged activation of the type I interferon (IFN-I) pathway leads to autoimmune diseases such as systemic lupus erythematosus (SLE). Metabolic regulation of cytokine signaling is critical for cellular homeostasis. Through metabolomics analyses of IFN-β-activated macrophages and an IFN-stimulated-response-element reporter screening, we identified spermine as a metabolite brake for Janus kinase (JAK) signaling. Spermine directly bound to the FERM and SH2 domains of JAK1 to impair JAK1-cytokine receptor interaction, thus broadly suppressing JAK1 phosphorylation triggered by cytokines IFN-I, IFN-II, interleukin (IL)-2, and IL-6. Peripheral blood mononuclear cells (PBMCs) from individuals with SLE showing decreased spermine concentrations exhibited enhanced IFN-I and lupus gene signatures. Spermine treatment attenuated autoimmune pathogenesis in SLE and psoriasis mice and reduced IFN-I signaling in monocytes from individuals with SLE. We synthesized a spermine derivative (spermine derivative 1 [SD1]) and showed that it had a potent immunosuppressive function. Our findings reveal spermine as a metabolic checkpoint for cellular homeostasis and a potential immunosuppressive molecule for controlling autoimmune disease.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"123 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141436022","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 : 2024-06-20DOI: 10.1016/j.immuni.2024.06.001
Randall T. Mertens, Aditya Misra, Peng Xiao, Seungbyn Baek, Joseph M. Rone, Davide Mangani, Kisha N. Sivanathan, Adedamola S. Arojojoye, Samuel G. Awuah, Insuk Lee, Guo-Ping Shi, Boryana Petrova, Jeannette R. Brook, Ana C. Anderson, Richard A. Flavell, Naama Kanarek, Martin Hemberg, Roni Nowarski
{"title":"A metabolic switch orchestrated by IL-18 and the cyclic dinucleotide cGAMP programs intestinal tolerance","authors":"Randall T. Mertens, Aditya Misra, Peng Xiao, Seungbyn Baek, Joseph M. Rone, Davide Mangani, Kisha N. Sivanathan, Adedamola S. Arojojoye, Samuel G. Awuah, Insuk Lee, Guo-Ping Shi, Boryana Petrova, Jeannette R. Brook, Ana C. Anderson, Richard A. Flavell, Naama Kanarek, Martin Hemberg, Roni Nowarski","doi":"10.1016/j.immuni.2024.06.001","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.06.001","url":null,"abstract":"<p>Tissues are exposed to diverse inflammatory challenges that shape future inflammatory responses. While cellular metabolism regulates immune function, how metabolism programs and stabilizes immune states within tissues and tunes susceptibility to inflammation is poorly understood. Here, we describe an innate immune metabolic switch that programs long-term intestinal tolerance. Intestinal interleukin-18 (IL-18) stimulation elicited tolerogenic macrophages by preventing their proinflammatory glycolytic polarization via metabolic reprogramming to fatty acid oxidation (FAO). FAO reprogramming was triggered by IL-18 activation of SLC12A3 (NCC), leading to sodium influx, release of mitochondrial DNA, and activation of stimulator of interferon genes (STING). FAO was maintained in macrophages by a bistable switch that encoded memory of IL-18 stimulation and by intercellular positive feedback that sustained the production of macrophage-derived 2′3′-cyclic GMP–AMP (cGAMP) and epithelial-derived IL-18. Thus, a tissue-reinforced metabolic switch encodes durable immune tolerance in the gut and may enable reconstructing compromised immune tolerance in chronic inflammation.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"80 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141430699","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 : 2024-06-19DOI: 10.1016/j.immuni.2024.05.024
Kelly A. Hagadorn, Mary E. Peterson, Hemanta Kole, Bethany Scott, Jeff Skinner, Ababacar Diouf, Eizo Takashima, Aissata Ongoiba, Safiatou Doumbo, Didier Doumtabe, Shanping Li, Padmapriya Sekar, Mei Yan, Chengsong Zhu, Hikaru Nagaoka, Bernard N. Kanoi, Quan-Zhen Li, Carole Long, Eric O. Long, Kassoum Kayentao, Christine S. Hopp
{"title":"Autoantibodies inhibit Plasmodium falciparum growth and are associated with protection from clinical malaria","authors":"Kelly A. Hagadorn, Mary E. Peterson, Hemanta Kole, Bethany Scott, Jeff Skinner, Ababacar Diouf, Eizo Takashima, Aissata Ongoiba, Safiatou Doumbo, Didier Doumtabe, Shanping Li, Padmapriya Sekar, Mei Yan, Chengsong Zhu, Hikaru Nagaoka, Bernard N. Kanoi, Quan-Zhen Li, Carole Long, Eric O. Long, Kassoum Kayentao, Christine S. Hopp","doi":"10.1016/j.immuni.2024.05.024","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.05.024","url":null,"abstract":"<p>Many infections, including malaria, are associated with an increase in autoantibodies (AAbs). Prior studies have reported an association between genetic markers of susceptibility to autoimmune disease and resistance to malaria, but the underlying mechanisms are unclear. Here, we performed a longitudinal study of children and adults (<em>n</em> = 602) in Mali and found that high levels of plasma AAbs before the malaria season independently predicted a reduced risk of clinical malaria in children during the ensuing malaria season. Baseline AAb seroprevalence increased with age and asymptomatic <em>Plasmodium falciparum</em> infection. We found that AAbs purified from the plasma of protected individuals inhibit the growth of blood-stage parasites and bind <em>P. falciparum</em> proteins that mediate parasite invasion. Protected individuals had higher plasma immunoglobulin G (IgG) reactivity against 33 of the 123 antigens assessed in an autoantigen microarray. This study provides evidence in support of the hypothesis that a propensity toward autoimmunity offers a survival advantage against malaria.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"14 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141425200","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 : 2024-06-18DOI: 10.1016/j.immuni.2024.05.023
Oliver T. Burton, Orian Bricard, Samar Tareen, Vaclav Gergelits, Simon Andrews, Laura Biggins, Carlos P. Roca, Carly Whyte, Steffie Junius, Aleksandra Brajic, Emanuela Pasciuto, Magda Ali, Pierre Lemaitre, Susan M. Schlenner, Harumichi Ishigame, Brian D. Brown, James Dooley, Adrian Liston
{"title":"The tissue-resident regulatory T cell pool is shaped by transient multi-tissue migration and a conserved residency program","authors":"Oliver T. Burton, Orian Bricard, Samar Tareen, Vaclav Gergelits, Simon Andrews, Laura Biggins, Carlos P. Roca, Carly Whyte, Steffie Junius, Aleksandra Brajic, Emanuela Pasciuto, Magda Ali, Pierre Lemaitre, Susan M. Schlenner, Harumichi Ishigame, Brian D. Brown, James Dooley, Adrian Liston","doi":"10.1016/j.immuni.2024.05.023","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.05.023","url":null,"abstract":"<p>The tissues are the site of many important immunological reactions, yet how the immune system is controlled at these sites remains opaque. Recent studies have identified Foxp3<sup>+</sup> regulatory T (Treg) cells in non-lymphoid tissues with unique characteristics compared with lymphoid Treg cells. However, tissue Treg cells have not been considered holistically across tissues. Here, we performed a systematic analysis of the Treg cell population residing in non-lymphoid organs throughout the body, revealing shared phenotypes, transient residency, and common molecular dependencies. Tissue Treg cells from different non-lymphoid organs shared T cell receptor (TCR) sequences, with functional capacity to drive multi-tissue Treg cell entry and were tissue-agnostic on tissue homing. Together, these results demonstrate that the tissue-resident Treg cell pool in most non-lymphoid organs, other than the gut, is largely constituted by broadly self-reactive Treg cells, characterized by transient multi-tissue migration. This work suggests common regulatory mechanisms may allow pan-tissue Treg cells to safeguard homeostasis across the body.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"40 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141334527","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":"High recallability of memory B cells requires ZFP318-dependent transcriptional regulation of mitochondrial function","authors":"Yifeng Wang, Wen Shao, Xin Liu, Qingtai Liang, Jiaqi Lei, Wenjuan Shi, Miao Mei, Ying Li, Xu Tan, Guocan Yu, Li Yu, Linqi Zhang, Hai Qi","doi":"10.1016/j.immuni.2024.05.022","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.05.022","url":null,"abstract":"<p>Expression of the transcriptional regulator ZFP318 is induced in germinal center (GC)-exiting memory B cell precursors and memory B cells (MBCs). Using a conditional ZFP318 fluorescence reporter that also enables ablation of ZFP318-expressing cells, we found that ZFP318-expressing MBCs were highly enriched with GC-derived cells. Although ZFP318-expressing MBCs constituted only a minority of the antigen-specific MBC compartment, their ablation severely impaired recall responses. Deletion of <em>Zfp318</em> did not alter the magnitude of primary responses but markedly reduced MBC participation in recall. CD40 ligation promoted <em>Zfp318</em> expression, whereas B cell receptor (BCR) signaling was inhibitory. Enforced ZFP318 expression enhanced recall performance of MBCs that otherwise responded poorly. ZFP318-deficient MBCs expressed less mitochondrial genes, had structurally compromised mitochondria, and were susceptible to reactivation-induced cell death. The abundance of ZFP318-expressing MBCs, instead of the number of antigen-specific MBCs, correlated with the potency of prime-boost vaccination. Therefore, ZFP318 controls the MBC recallability and represents a quality checkpoint of humoral immune memory.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"352 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141333819","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 : 2024-06-13DOI: 10.1016/j.immuni.2024.05.019
Nadège Nziza, Wonyeong Jung, Maanasa Mendu, Tina Chen, Boris Julg, Barney Graham, Octavio Ramilo, Asuncion Mejias, Galit Alter
{"title":"Longitudinal humoral analysis in RSV-infected infants identifies pre-existing RSV strain-specific G and evolving cross-reactive F antibodies","authors":"Nadège Nziza, Wonyeong Jung, Maanasa Mendu, Tina Chen, Boris Julg, Barney Graham, Octavio Ramilo, Asuncion Mejias, Galit Alter","doi":"10.1016/j.immuni.2024.05.019","DOIUrl":"https://doi.org/10.1016/j.immuni.2024.05.019","url":null,"abstract":"<p>Respiratory syncytial virus (RSV) is among the most common causes of lower respiratory tract infection (LRTI) and hospitalization in infants. However, the mechanisms of immune control in infants remain incompletely understood. Antibody profiling against attachment (G) and fusion (F) proteins in children less than 2 years of age, with mild (outpatients) or severe (inpatients) RSV disease, indicated substantial age-dependent differences in RSV-specific immunity. Maternal antibodies were detectable for the first 3 months of life, followed by a long window of immune vulnerability between 3 and 6 months and a rapid evolution of FcγR-recruiting immunity after 6 months of age. Acutely ill hospitalized children exhibited lower G-specific antibodies compared with healthy controls. With disease resolution, RSV-infected infants generated broad functional RSV strain-specific G-responses and evolved cross-reactive F-responses, with minimal maternal imprinting. These data suggest an age-independent RSV G-specific functional humoral correlate of protection, and the evolution of RSV F-specific functional immunity with disease resolution.</p>","PeriodicalId":13269,"journal":{"name":"Immunity","volume":"34 1","pages":""},"PeriodicalIF":32.4,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141315884","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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