Science Immunology最新文献_第2页

Fibroblastic reticular cells form reactive myeloid cell niches in human lymph nodes 成纤维网状细胞在人淋巴结中形成反应性骨髓细胞壁龛

IF 17.6 1区医学

Science Immunology Pub Date : 2025-05-02 DOI: 10.1126/sciimmunol.ads6820

Mechthild Lütge, Lisa Kurz, Yves Stanossek, Samuel Meili, Hung-Wei Cheng, Angelina De Martin, Joshua Brandstadter, Ivan Maillard, Mark D. Robinson, Sandro J. Stoeckli, Natalia B. Pikor, Lucas Onder, Burkhard Ludewig

{"title":"Fibroblastic reticular cells form reactive myeloid cell niches in human lymph nodes","authors":"Mechthild Lütge, Lisa Kurz, Yves Stanossek, Samuel Meili, Hung-Wei Cheng, Angelina De Martin, Joshua Brandstadter, Ivan Maillard, Mark D. Robinson, Sandro J. Stoeckli, Natalia B. Pikor, Lucas Onder, Burkhard Ludewig","doi":"10.1126/sciimmunol.ads6820","DOIUrl":"10.1126/sciimmunol.ads6820","url":null,"abstract":"<div >Lymph nodes play a key role in maintaining fluid balance in homeostatic and inflamed tissues and provide fibroblastic niche environments for optimal immune cell positioning and interaction. Here, we used single-cell and spatial transcriptomic analyses in combination with high-resolution imaging to molecularly define and functionally characterize niche-forming cells that control inflammation-driven remodeling in human lymph nodes. Fibroblastic reticular cells responded to inflammatory perturbation with activation and expansion of poised niche environments. Inflammation-induced adaptation of lymph node infrastructure and topography included the expansion of peptidase inhibitor 16 (PI16)–expressing reticular cell (PI16+ RC) networks that enwrap the perivenular conduit system. Interactome analyses indicated that macrophage-derived oncostatin M directs PI16+ RC activation in inflamed lymph nodes and thereby promotes immune cell aggregation in the perivenular space. In conclusion, these data demonstrate that the inflammatory remodeling of human lymph nodes results in the formation of reactive myeloid cell niches by PI16+ RCs.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 107","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads6820","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143898138","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}

引用次数: 0

Clone tracking through repeated malaria identifies high-fidelity memory CD4 T cell responses 通过重复疟疾克隆跟踪识别高保真记忆CD4 T细胞反应

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-25 DOI: 10.1126/sciimmunol.ads2957

Jason Nideffer, Florian Bach, Felistas Nankya, Kenneth Musinguzi, Šimon Borna, Michelle Mantilla, Maato Zedi, Aracely Garcia Romero, Chloe Gerungan, Nora Yang, Soyeon Kim, Kattria van der Ploeg, Kylie Camanag, Luis Lopez, Evelyn Nansubuga, Joaniter I. Nankabirwa, Emmanuel Arinaitwe, Potchara Boonrat, Steven Strubbe, Alma-Martina Cepika, Saki Takahashi, Grant Dorsey, Bryan Greenhouse, Isabel Rodriguez-Barraquer, Moses R. Kamya, Rosa Bacchetta, Isaac Ssewanyana, Ashraful Haque, Maria Grazia Roncarolo, Prasanna Jagannathan

{"title":"Clone tracking through repeated malaria identifies high-fidelity memory CD4 T cell responses","authors":"Jason Nideffer, Florian Bach, Felistas Nankya, Kenneth Musinguzi, Šimon Borna, Michelle Mantilla, Maato Zedi, Aracely Garcia Romero, Chloe Gerungan, Nora Yang, Soyeon Kim, Kattria van der Ploeg, Kylie Camanag, Luis Lopez, Evelyn Nansubuga, Joaniter I. Nankabirwa, Emmanuel Arinaitwe, Potchara Boonrat, Steven Strubbe, Alma-Martina Cepika, Saki Takahashi, Grant Dorsey, Bryan Greenhouse, Isabel Rodriguez-Barraquer, Moses R. Kamya, Rosa Bacchetta, Isaac Ssewanyana, Ashraful Haque, Maria Grazia Roncarolo, Prasanna Jagannathan","doi":"10.1126/sciimmunol.ads2957","DOIUrl":"10.1126/sciimmunol.ads2957","url":null,"abstract":"<div >Few studies have tracked human CD4+ T cell clones through repeated infections. We used longitudinal single-cell RNA and T cell receptor (TCR) tracking to study the functional stability and memory potential of CD4+ T cell clonotypes during repeated Plasmodium falciparum (Pf) infections in Ugandan children and adults. Nearly all clonotypes displayed a strong preference for one of seven CD4+ subsets. This phenomenon of “clonal fidelity” was influenced by clonal expansion, linking T cell polarization and proliferation in vivo. Using clone tracking, we characterized subset-specific activation trajectories and identified antigen-specific clones. Type 1 regulatory T (TR1) cells accounted for nearly 90% of Pf-specific CD4+ T cells in blood. Tracking these clones longitudinally for hundreds of days, we observed malaria-induced expansion of TR1 effectors, long-term persistence of TR1 memory cells, and high-fidelity recall responses after reinfection. This work establishes clonal fidelity as a natural phenomenon and demonstrates the stable, long-term memory potential of TR1 cells.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads2957","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872828","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}

引用次数: 0

T–B cell cooperation in ectopic lymphoid follicles propagates CNS autoimmunity T-B细胞在异位淋巴滤泡中的合作促进中枢神经系统自身免疫

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-25 DOI: 10.1126/sciimmunol.adn2784

Anna Kolz, Clara de la Rosa, Isabel J. Syma, Sarah McGrath, Vladyslav Kavaka, Rosa Schmitz, Anna S. Thomann, Martin Kerschensteiner, Eduardo Beltran, Naoto Kawakami, Anneli Peters

{"title":"T–B cell cooperation in ectopic lymphoid follicles propagates CNS autoimmunity","authors":"Anna Kolz, Clara de la Rosa, Isabel J. Syma, Sarah McGrath, Vladyslav Kavaka, Rosa Schmitz, Anna S. Thomann, Martin Kerschensteiner, Eduardo Beltran, Naoto Kawakami, Anneli Peters","doi":"10.1126/sciimmunol.adn2784","DOIUrl":"10.1126/sciimmunol.adn2784","url":null,"abstract":"<div >Meningeal ectopic lymphoid follicle (eLF)–like structures have been described in multiple sclerosis, but their role in central nervous system (CNS) autoimmunity is unclear. Here, we used a T helper 17 (TH17) adoptive transfer experimental autoimmune encephalomyelitis model featuring formation of eLFs. Single-cell RNA sequencing revealed that clusters of activated B cells and B1/marginal zone–like B cells were overrepresented in the CNS and identified B cells poised for undergoing germinal center reactions and clonal expansion in the CNS. Using intravital imaging to directly visualize TH17–B cell interactions, we demonstrated that T and B cells form long-lasting antigen-specific contacts in meningeal eLFs that result in reactivation of autoreactive T cells. CNS T cells depended on CNS B cells to maintain a proinflammatory cytokine profile. Our study reveals that extensive T–B cell cooperation occurs in meningeal eLFs, promoting both B cell differentiation and T cell reactivation, and may thereby propagate smoldering inflammation in the CNS.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143872827","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}

引用次数: 0

Erratum for the Research Article “IL-4 induces CD22 expression to restrain the effector program of virtual memory T cells” by B. Yang et al. B. Yang等研究文章《IL-4诱导CD22表达抑制虚拟记忆T细胞效应程序》的误读

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-25 DOI: 10.1126/sciimmunol.adx9360

引用次数: 0

CCR8+ decidual regulatory T cells maintain maternal-fetal immune tolerance during early pregnancy CCR8 +个体调节性T细胞在妊娠早期维持母胎免疫耐受

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-18 DOI: 10.1126/sciimmunol.ado2463

Zhuqing Li, Pinxin Si, Tingting Meng, Xiaoran Zhao, Chendi Zhu, Dunfang Zhang, Shutong Meng, Nianyu Li, Ran Liu, Tianxiang Ni, Junhao Yan, Hongchang Li, Ning Zhao, Chao Zhong, Yingying Qin, WanJun Chen, Zi-Jiang Chen, Xue Jiao

{"title":"CCR8+ decidual regulatory T cells maintain maternal-fetal immune tolerance during early pregnancy","authors":"Zhuqing Li, Pinxin Si, Tingting Meng, Xiaoran Zhao, Chendi Zhu, Dunfang Zhang, Shutong Meng, Nianyu Li, Ran Liu, Tianxiang Ni, Junhao Yan, Hongchang Li, Ning Zhao, Chao Zhong, Yingying Qin, WanJun Chen, Zi-Jiang Chen, Xue Jiao","doi":"10.1126/sciimmunol.ado2463","DOIUrl":"10.1126/sciimmunol.ado2463","url":null,"abstract":"<div >Regulatory T (Treg) cells play a vital role in maintaining maternal immune tolerance to the semiallogeneic fetus during pregnancy. Treg cell population heterogeneity and tissue-specific functions in the human decidua remain largely unknown. Here, using single-cell transcriptomic and T cell receptor sequencing of human CD4+ T cells from first-trimester deciduae and matched peripheral blood of pregnant women, we identified a highly activated, immunosuppressive CCR8+ Treg cell subset specifically enriched in the decidua (dTreg cells). CCR8+ dTreg cells were decreased in patients with recurrent pregnancy loss (RPL) and an abortion-prone mouse model. Depletion of CCR8+ dTreg cells increased susceptibility to fetal loss, with altered decidual immune profiles. Adoptive transfer of CCR8+ Treg cells rescued fetal loss in abortion-prone mice. The CCR8 ligand CCL1 was mainly produced by decidual CD49a+ natural killer cells and was significantly decreased in patients with RPL. Our data demonstrate that CCR8+ dTreg cells are required to maintain maternal-fetal tolerance and highlight potential avenues for RPL therapies.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ado2463","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847070","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}

引用次数: 0

Endothelial-driven TGFβ signaling supports lung interstitial macrophage development from monocytes 内皮驱动的tgf - β信号支持肺间质巨噬细胞从单核细胞发育而来

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-18 DOI: 10.1126/sciimmunol.adr4977

Wen Peng, Domien Vanneste, David Bejarano, Joan Abinet, Margot Meunier, Coraline Radermecker, Fabienne Perin, Didier Cataldo, Fabrice Bureau, Andreas Schlitzer, Qiang Bai, Thomas Marichal

{"title":"Endothelial-driven TGFβ signaling supports lung interstitial macrophage development from monocytes","authors":"Wen Peng, Domien Vanneste, David Bejarano, Joan Abinet, Margot Meunier, Coraline Radermecker, Fabienne Perin, Didier Cataldo, Fabrice Bureau, Andreas Schlitzer, Qiang Bai, Thomas Marichal","doi":"10.1126/sciimmunol.adr4977","DOIUrl":"10.1126/sciimmunol.adr4977","url":null,"abstract":"<div >Lung interstitial macrophages (IMs) are monocyte-derived parenchymal macrophages whose tissue-supportive functions remain unclear. Despite progress in understanding lung IM diversity and transcriptional regulation, the signals driving their development from monocytes and their functional specification remain unknown. Here, we found that lung endothelial cell–derived Tgfβ1 triggered a core Tgfβ receptor–dependent IM signature in mouse bone marrow–derived monocytes. Myeloid-specific impairment of Tgfβ receptor signaling severely disrupted monocyte-to-IM development, leading to the accumulation of perivascular immature monocytes, reduced IM numbers, and a loss of IM-intrinsic identity, a phenomenon similarly observed in the absence of endothelial-specific Tgfβ1. Mice lacking the Tgfβ receptor in monocytes and IMs exhibited altered monocyte and IM niche occupancy and hallmarks of aging including impaired immunoregulation, hyperinflation, and fibrosis. Our work identifies a Tgfβ signaling–dependent endothelial-IM axis that shapes IM development and sustains lung integrity, providing foundations for IM-targeted interventions in aging and chronic inflammation.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847064","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}

引用次数: 0

Erratum for the Research Article “Anti–immune complex antibodies are elicited during repeated immunization with HIV Env immunogens” by S. Brown et al. S. Brown等人的研究文章“在HIV Env免疫原反复免疫期间引发抗免疫复合物抗体”的勘误。

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-11 DOI: 10.1126/sciimmunol.adx6798

引用次数: 0

Foxo1 regulates intestinal tissue–resident memory CD8 T cell biology in an anatomic compartment– and context-specific manner Foxo1以解剖室和上下文特异性的方式调节肠组织驻留记忆CD8 T细胞生物学

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-11 DOI: 10.1126/sciimmunol.adn1894

Paul Hsu, Eunice J. Choi, William H. Wong, Yun Hsuan Lin, Sara A. Vandenburgh, Yi Chia Liu, Priscilla Yao, Cynthia S. Indralingam, Gene W. Yeo, Elina I. Zuniga, Ananda W. Goldrath, Wei Wang, John T. Chang

{"title":"Foxo1 regulates intestinal tissue–resident memory CD8 T cell biology in an anatomic compartment– and context-specific manner","authors":"Paul Hsu, Eunice J. Choi, William H. Wong, Yun Hsuan Lin, Sara A. Vandenburgh, Yi Chia Liu, Priscilla Yao, Cynthia S. Indralingam, Gene W. Yeo, Elina I. Zuniga, Ananda W. Goldrath, Wei Wang, John T. Chang","doi":"10.1126/sciimmunol.adn1894","DOIUrl":"10.1126/sciimmunol.adn1894","url":null,"abstract":"<div >Tissue-resident memory CD8 T (TRM) cells serve as a front-line defense against microbial pathogens in barrier and mucosal tissues. Accurately predicting the roles of tissue-specific transcription factors (TFs) that regulate TRM biology remains a challenge. Here, by applying integrated transcriptomic and epigenomic analyses, we have identified an unexpected role for forkhead box O1 (Foxo1), a TF previously known to regulate circulating memory T cells, in intestinal TRM biology. Foxo1 repressed the maintenance of early small intestinal intraepithelial TRM cells in contrast with its actions in sustaining TRM cells from small intestinal lamina propria and colon and contrary to its broader role in promoting intestinal TRM cell formation. These findings highlight the emerging concept that the transcriptional regulation of TRM cells may be more complex and nuanced than previously appreciated and underscore the utility of integrated transcriptomic and epigenomic analyses in reconstructing TF-regulatory networks.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822349","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}

引用次数: 0

Bcl11a maintains hematopoietic stem cell function but accelerates inflammation-driven exhaustion during aging Bcl11a维持造血干细胞功能，但在衰老过程中加速炎症驱动的衰竭

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-11 DOI: 10.1126/sciimmunol.adr2041

Jing Wang, Linlin Zhang, Xinyu Cui, Xiang Xu, Rui Guo, Kairui Li, Li Zhang, Bing Xu, Cizhong Jiang, Yong Yu

{"title":"Bcl11a maintains hematopoietic stem cell function but accelerates inflammation-driven exhaustion during aging","authors":"Jing Wang, Linlin Zhang, Xinyu Cui, Xiang Xu, Rui Guo, Kairui Li, Li Zhang, Bing Xu, Cizhong Jiang, Yong Yu","doi":"10.1126/sciimmunol.adr2041","DOIUrl":"10.1126/sciimmunol.adr2041","url":null,"abstract":"<div >Preserving hematopoietic stem cell (HSC) functionality is essential for maintaining healthy blood and the immune system throughout life. HSC function declines with age; however, the underlying mechanisms are not fully understood. Using an inducible mosaic mouse model to overexpress the transcription factor Bcl11a in the hematopoietic compartment, we found that an aging-related increase in Bcl11a mitigated HSC functional decline, promoted IL-1β production in the bone marrow (BM), and accelerated HSC attrition in a non–cell-autonomous manner. Aging-related inflammation in the BM enhanced Bcl11a and Fc receptor (FcR) expression in HSCs, and FcR signaling induced HSC differentiation. This was counteracted by Bcl11a through repression of Fcer1g. Bcl11a up-regulation promoted IL-1β production in BM myeloid cells, driving inflammation and HSC deterioration. Deletion of Fcer1g, or blocking IL-1β signaling, eliminated this non–cell-autonomous effect on HSC decline. These findings demonstrate that Bcl11a plays a dual role in HSCs during aging not only by cell-intrinsically preserving HSC function but also by promoting BM inflammation and HSC dysfunction.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822343","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}

引用次数: 0

Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts 心理应激通过TGFβ抑制免疫作用成纤维细胞的作用增加皮肤感染

IF 17.6 1区医学

Science Immunology Pub Date : 2025-04-11 DOI: 10.1126/sciimmunol.ads0519

Hung Chan, Fengwu Li, Tatsuya Dokoshi, Kellen J. Cavagnero, Qing Li, Yang Chen, Carlos Aguilera, Teruaki Nakatsuji, Edward Liu, Aaryan Indra, Daping Yang, Ottaviani Valentina, Tomofumi Numata, Brittany Crown, Henry Li, Kevin J. Williams, Isaac M. Chiu, Steven J. Bensinger, WanJun Chen, Richard L. Gallo

{"title":"Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts","authors":"Hung Chan, Fengwu Li, Tatsuya Dokoshi, Kellen J. Cavagnero, Qing Li, Yang Chen, Carlos Aguilera, Teruaki Nakatsuji, Edward Liu, Aaryan Indra, Daping Yang, Ottaviani Valentina, Tomofumi Numata, Brittany Crown, Henry Li, Kevin J. Williams, Isaac M. Chiu, Steven J. Bensinger, WanJun Chen, Richard L. Gallo","doi":"10.1126/sciimmunol.ads0519","DOIUrl":"10.1126/sciimmunol.ads0519","url":null,"abstract":"<div >Infections after psychological stress are a major health care problem. Single-cell transcriptomics and lipidomic profiling in a mouse model of stress show that dermal fibroblasts undergoing adipogenesis have defective responses to Staphylococcus aureus skin infection. Adrenalectomy or adrenergic inhibition restores the fibroblast adipogenic response to S. aureus and enables mice to effectively resist infection during stress. Increased susceptibility to S. aureus from stress is attributed to suppression of the antimicrobial peptide cathelicidin (Camp) because adrenaline directly inhibits Camp production by fibroblasts, and mice lacking Camp in fibroblasts do not increase infection after stress. Transforming growth factor β (TGFβ) is induced by stress and adrenergic signaling, and inhibition of TGFβ or deletion of the TGFβ receptor on fibroblasts increases Camp expression and restores protection against infection. Together, these data show that stress initiates a brain-skin axis mediated by TGFβ that impairs the immune defense function of dermal fibroblasts to produce the Camp antimicrobial peptide.</div>","PeriodicalId":21734,"journal":{"name":"Science Immunology","volume":"10 106","pages":""},"PeriodicalIF":17.6,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.science.org/doi/reader/10.1126/sciimmunol.ads0519","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143822348","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}

引用次数: 0