Journal of Leukocyte Biology最新文献_第4页

Substance P regulates memory Th17 cell generation and maintenance in chronic dry eye disease. P 物质调节慢性干眼症中 Th17 记忆细胞的生成和维持。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-27 DOI: 10.1093/jleuko/qiae142

Shudan Wang, Amirreza Naderi, Francesca Kahale, Gustavo Ortiz, Katayoon Forouzanfar, Yihe Chen, Reza Dana

{"title":"Substance P regulates memory Th17 cell generation and maintenance in chronic dry eye disease.","authors":"Shudan Wang, Amirreza Naderi, Francesca Kahale, Gustavo Ortiz, Katayoon Forouzanfar, Yihe Chen, Reza Dana","doi":"10.1093/jleuko/qiae142","DOIUrl":"10.1093/jleuko/qiae142","url":null,"abstract":"Substance P is a neuropeptide expressed by nerves and an array of cells that serves as a critical mediator of neuroinflammation. Our recent work has demonstrated that blocking the preferred receptor for substance P, neurokinin 1 receptor, effectively suppresses the induction of acute dry eye disease by preserving regulatory T-cell function, while inhibiting antigen-presenting cell maturation and subsequent generation of effector Th17 cells. Clinically, dry eye disease is a chronic disorder characterized by sustained ocular surface inflammation, which is mediated by long-lived memory Th17 cells demonstrated in our well-established chronic dry eye disease model. The present study aimed to further understand the function of substance P in the chronic phase of dry eye disease and its role in regulating the underlying pathogenic memory Th17. In vitro culture of effector T cells isolated from acute dry eye disease with substance P led to an enhanced conversion of effector Th17 to memory Th17, while culturing memory T cells isolated from chronic dry eye disease with substance P effectively preserved the memory Th17 cells. In contrast, the addition of a neurokinin 1 receptor antagonist in the cultures abolished the substance P-mediated effects. Furthermore, in vivo treatment with the neurokinin 1 receptor antagonist during the resolution phase of acute dry eye disease significantly suppressed memory Th17 generation, and treatment in the chronic phase of dry eye disease disrupted the maintenance of memory Th17. Taken together, our results demonstrate that increased expression of substance P promotes memory Th17 generation and maintenance in chronic dry eye disease, and thus blockade of substance P represents a novel promising memory Th17-targeting strategy in treating chronic ocular surface inflammation.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":"1446-1453"},"PeriodicalIF":3.6,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11599119/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450692","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}

引用次数: 0

Advancing toward a unified eosinophil signature from transcriptional profiling. 从转录谱分析中获得统一的嗜酸性粒细胞特征。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-27 DOI: 10.1093/jleuko/qiae188

Krishan D Chhiba, Fei Li Kuang

{"title":"Advancing toward a unified eosinophil signature from transcriptional profiling.","authors":"Krishan D Chhiba, Fei Li Kuang","doi":"10.1093/jleuko/qiae188","DOIUrl":"10.1093/jleuko/qiae188","url":null,"abstract":"Eosinophils are granulocytes that can accumulate in increased numbers in tissues and/or peripheral blood in disease. Phenotyping of eosinophils in health and disease has the potential to improve the precision of diagnosis and choice of therapies for eosinophilic-associated diseases. Transcriptional profiling of eosinophils has been plagued by cell fragility and difficulty isolating high-quality RNA. With several technological advances, single-cell RNA sequencing has become possible with eosinophils, at least from mice, while bulk RNA sequencing and microarrays have been performed in both murine and human samples. Anticipating more eosinophil transcriptional profiles in the coming years, we provide a summary of prior studies conducted on mouse and human eosinophils in blood and tissue, with a discussion of the advantages and potential pitfalls of various approaches. Common technical standards in studying eosinophil biology would help advance the field and make cross-study comparisons possible. Knowledge gaps and opportunities include identifying a minimal set of genes that define the eosinophil lineage, comparative studies between active disease and remission vs. homeostasis or development, especially in humans, and a comprehensive comparison between murine and human eosinophils at the transcriptional level. Characterizing such transcriptional patterns will be important to understanding the complex and diverse roles of eosinophils in both health and disease.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":"1324-1333"},"PeriodicalIF":3.6,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11602342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108186","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}

引用次数: 0

SUMO-specific protease 1 exacerbates acute myeloid leukemia by enhancing beclin 1-dependent autophagy through polypyrimidine tract-binding protein 1 deSUMOylation. SENP1 通过 PTBP1 deSUMOylation 增强 BECN1 依赖性自噬，从而加剧急性髓性白血病。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-27 DOI: 10.1093/jleuko/qiae143

Lina Xing, Xuefei Guo, Xiaolei Zhang, Ying Wang, Jinhai Ren

{"title":"SUMO-specific protease 1 exacerbates acute myeloid leukemia by enhancing beclin 1-dependent autophagy through polypyrimidine tract-binding protein 1 deSUMOylation.","authors":"Lina Xing, Xuefei Guo, Xiaolei Zhang, Ying Wang, Jinhai Ren","doi":"10.1093/jleuko/qiae143","DOIUrl":"10.1093/jleuko/qiae143","url":null,"abstract":"Genetic association between SUMO-specific protease 1 (SENP1) and acute myeloid leukemia (AML) has been validated. However, the mechanism by which SENP1 affects AML proliferation, apoptosis, and autophagy remains unknown. The levels of SENP1 and polypyrimidine tract-binding protein 1 (PTBP1) were measured in patients with AML, AML cell lines, and xenograft tissues. The effects of SENP1 on AML proliferation, apoptosis, and beclin 1 (BECN1)-dependent autophagy were assessed through in vitro and in vivo loss- or gain-of-function experiments. SUMOylation analysis using immunoprecipitation (IP), RNA pull-down, RNA IP (RIP), and RNA stability assays were used to explore the molecular mechanism of SENP1 in AML development. The SENP1 level was elevated in AML samples. Silencing SENP1 impeded the development of AML, as evidenced by the inhibition of proliferation and promotion of G1-phase arrest and apoptosis resulting from SENP1 depletion in AML cells. Moreover, silencing of SENP1 restrained BECN1-depentent autophagy in AML cells. In addition, the overexpression of BECN1 or PTBP1 partially neutralized the effect of SENP1 knockdown on AML cell behavior. Mechanistically, SENP1 mediated PTBP1 deSUMOylation, which then directly interacted with BECN1 mRNA and enhanced its stability. In vivo experiments further confirmed the repressive effects of SENP1 suppression on AML development. Collectively, the SENP1/PTBP1/BECN1 signaling axis has been identified as a significant therapeutic target for enhancing AML treatment.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":"1454-1468"},"PeriodicalIF":3.6,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457410","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}

引用次数: 0

Neutrophils on the mast cell menu. 肥大细胞菜单上的中性粒细胞

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-27 DOI: 10.1093/jleuko/qiae221

Eric Espinosa

引用次数: 0

Transgenic αβ TCR tonic signaling is leukemogenic while strong stimulation is leukemia-suppressive. 转基因αβ TCR强直信号具有致白血病性，而强刺激则具有抑制白血病性。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-22 DOI: 10.1093/jleuko/qiae249

Telmo A Catarino, Ivette Pacheco-Leyva, Marina Baessa, João L Pereira, Nuno R Dos Santos

{"title":"Transgenic αβ TCR tonic signaling is leukemogenic while strong stimulation is leukemia-suppressive.","authors":"Telmo A Catarino, Ivette Pacheco-Leyva, Marina Baessa, João L Pereira, Nuno R Dos Santos","doi":"10.1093/jleuko/qiae249","DOIUrl":"https://doi.org/10.1093/jleuko/qiae249","url":null,"abstract":"The pre-T cell receptor (TCR) and TCR complexes are frequently expressed in T-cell acute lymphoblastic leukemia (T-ALL), an aggressive T cell precursor malignancy. Although mutations in TCR components are infrequent in T-ALL, earlier research indicated that transgenic αβ TCR expression in mouse T cell precursors promoted T-ALL development. However, we recently found that stimulation of TCR signaling in T-ALL induced leukemic cell apoptosis and suppressed leukemia. Our aim was to elucidate if a given αβ TCR complex has a dual role in leukemogenesis depending on the nature of the stimulus. We demonstrate that transgenic expression of the Marilyn αβ TCR, specific for the H-Y male antigen presented by major histocompatibility complex class II, triggers T-ALL development exclusively in female mice. This T-ALL exhibited Notch1 mutations, Cdkn2a copy number loss, immature immunophenotype and infiltrated both lymphoid and non-lymphoid organs. Furthermore, leukemic cells expressed surface CD5, a marker of tonic TCR signaling. T-ALL efficiently developed in Rag2-deficient Marilyn transgenic females, indicating that Rag2-mediated recombination is not implicated in this T-ALL model. T-ALL development was also observed in the OT-I TCR transgenic mouse model, but it did not occur when MHC class I was abrogated through genetic inactivation of β2-microglobulin. Remarkably, exposure of Marilyn female T-ALL cells to endogenous agonist antigen in male recipient mice or exogenous peptide in female recipient mice resulted in T-ALL apoptosis and prolonged mouse survival. These findings underscore the dual role of the same αβ TCR complex in T-ALL, where tonic stimulation is leukemogenic, while strong stimulation suppresses leukemia.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687140","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}

引用次数: 0

The tumor-neutrophil interactions in the microenvironment of brain metastases with different primary sites. 不同原发部位脑转移瘤微环境中肿瘤与中性粒细胞的相互作用。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-20 DOI: 10.1093/jleuko/qiae248

Tamer A Kaya, Klaus-Peter Stein, Anna Schaufler, Belal Neyazi, Ali Rashidi, Ulf D Kahlert, Christian Mawrin, I Erol Sandalcioglu, Claudia A Dumitru

{"title":"The tumor-neutrophil interactions in the microenvironment of brain metastases with different primary sites.","authors":"Tamer A Kaya, Klaus-Peter Stein, Anna Schaufler, Belal Neyazi, Ali Rashidi, Ulf D Kahlert, Christian Mawrin, I Erol Sandalcioglu, Claudia A Dumitru","doi":"10.1093/jleuko/qiae248","DOIUrl":"https://doi.org/10.1093/jleuko/qiae248","url":null,"abstract":"Brain metastases (BrM) originating from lung and breast cancer can recruit and activate neutrophils to acquire a tumor-promoting phenotype. It is currently unclear if this phenomenon also occurs in BrM arising from other primary sites. Here, we investigated the effect of tumor cells isolated from melanoma, lung and gastrointestinal (GI) cancer BrM on neutrophil biology and functions. We found that lung and GI, but not melanoma BrM cells produced CXCL8/IL-8, and promoted neutrophil recruitment. Similarly, lung and GI, but not melanoma BrM cells, prolonged the survival of neutrophils, and stimulated them to release MMP9 and CCL4/MIP1β. In situ, lung and GI BrM tissues contained significantly higher numbers of tumor-infiltrating neutrophils compared to melanoma BrM. The levels of neutrophil infiltration significantly correlated with the proliferation index of these tumors. Our findings identify variabilities in the immune microenvironment of BrM with different primary sites, which may ultimately affect their pathophysiology and progression.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681884","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}

引用次数: 0

Cannabinoid Receptor type 2 agonist GP1a attenuates macrophage activation induced by M. bovis-BCG by inhibiting NF-ĸB signaling. 大麻素受体2型激动剂GP1a通过抑制NF-ĸB信号传导来减轻牛乳杆菌-BCG诱导的巨噬细胞活化。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-14 DOI: 10.1093/jleuko/qiae246

Jessica Do Prado Valeriano, Magaiver Andrade-Silva, Filipe Pereira-Dutra, Leonardo Noboru Seito, Patricia Torres Bozza, Elaine Cruz Rosas, Maria Fernanda de Souza Costa, Maria das Graças Henriques

{"title":"Cannabinoid Receptor type 2 agonist GP1a attenuates macrophage activation induced by M. bovis-BCG by inhibiting NF-ĸB signaling.","authors":"Jessica Do Prado Valeriano, Magaiver Andrade-Silva, Filipe Pereira-Dutra, Leonardo Noboru Seito, Patricia Torres Bozza, Elaine Cruz Rosas, Maria Fernanda de Souza Costa, Maria das Graças Henriques","doi":"10.1093/jleuko/qiae246","DOIUrl":"https://doi.org/10.1093/jleuko/qiae246","url":null,"abstract":"Tuberculosis (TB) is one of the leading causes of death worldwide and a major public health problem. Immune evasion mechanisms and antibiotic resistance highlight the need to better understand this disease and explore alternative treatment approaches. Mycobacterial infection modulates the macrophage response and metabolism to persist and proliferate inside the cell. Cannabinoid receptor type 2 (CB2) is expressed mainly in leukocytes and modulates the course of inflammatory diseases. Therefore, our study aimed to evaluate the effects of the CB2-selective agonist GP1a on irradiated M. bovis-BCG (iBCG)-induced J774A.1 macrophage activation. We observed increased expression of CB2 in macrophages after iBCG stimulation. The pretreatment with CB2-agonists, GP1a, JWH-133, and GW-833972A (10 µM), reduced iBCG-induced TNF-α and IL-6 release by these cells. Moreover, the CB2-antagonist AM630 (200nM) treatment confirmed the activity of GP1a on CB2 by scale down its effect on cytokine production. GP1a pretreatment (10 µM) also inhibited the iBCG-induced production of inflammatory mediators as prostaglandin (PG)E2 and nitric oxide (NO) by macrophages. Additionally, GP1a pretreatment also reduced the transcription of proinflammatory genes (inos, il1b, cox2) and genes related to lipid metabolism (dgat1, acat1, plin2, atgl, cd36). Indeed, lipid droplet accumulation was reduced by GP1a treatment which was partially blockade by AM630 pretreatment. Finally, GP1a pretreatment reduced the activation of the NF-κB signaling pathway. In conclusion, the activation of CB2 by GP1a modulated the macrophage response to iBCG by reducing inflammatory mediator levels and metabolic reprogramming.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621926","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}

引用次数: 0

Erratum for "Optimizing a 5-factor cocktail to prepare reparative macrophages for wound healing". 为 "优化 5 因子鸡尾酒，为伤口愈合准备修复巨噬细胞 "撰写的勘误。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-13 DOI: 10.1093/jleuko/qiae238

引用次数: 0

Interleukin-10 inhibits important components of trained immunity in human monocytes. 白细胞介素-10 可抑制人类单核细胞中训练有素的免疫力的重要组成部分。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-12 DOI: 10.1093/jleuko/qiae240

Rutger J Röring, Flavia Scognamiglio, Lisanne C de Jong, Laszlo A Groh, Vasiliki Matzaraki, Valerie A C M Koeken, Leo A B Joosten, Athanasios Ziogas, Mihai G Netea

{"title":"Interleukin-10 inhibits important components of trained immunity in human monocytes.","authors":"Rutger J Röring, Flavia Scognamiglio, Lisanne C de Jong, Laszlo A Groh, Vasiliki Matzaraki, Valerie A C M Koeken, Leo A B Joosten, Athanasios Ziogas, Mihai G Netea","doi":"10.1093/jleuko/qiae240","DOIUrl":"https://doi.org/10.1093/jleuko/qiae240","url":null,"abstract":"Trained immunity induces antigen-agnostic enhancement of host defense and protection against secondary infections, but inappropriate activation can contribute to the pathophysiology of inflammatory diseases. Tight regulation of trained immunity is therefore needed to avoid pathology, but little is known about the endogenous processes that modulate it. Here, we investigated the potential of IL-10, a prototypical anti-inflammatory cytokine, to inhibit trained immunity. IL-10 induced tolerance and inhibited trained immunity in primary human monocytes at both functional and transcriptional levels. Inhibition of STAT3, a signaling route that mediates IL-10 signals, induced trained immunity. IL-10 downregulated glycolytic and oxidative metabolism in monocytes, but did not impact the metabolic effects of β-glucan-induced trained immunity. Furthermore, IL-10 prevented increased ROS production in BCG-induced training, but did not influence phagocytosis upregulation. In a cohort study of healthy volunteers vaccinated with BCG, genetic variants that influenced IL-10 or its receptor modulated BCG-induced trained immunity. Furthermore, circulating IL-10 concentrations were negatively correlated with induction of trained immunity after BCG vaccination in a sex-specific manner. In conclusion, IL-10 inhibited several, albeit not all, immunological functions amplified after induction of trained immunity. Follow-up studies should explore the precise molecular mechanism that mediate the effects of IL-10 on trained immunity. Addressing these knowledge gaps is an important step towards optimizing IL-10's potential as a therapeutic target in diseases characterized by inappropriate induction of trained immunity.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621940","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}

引用次数: 0

Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans. 中性粒细胞蜂拥对限制白色念珠菌的口腔黏膜感染至关重要。

IF 3.6 3区医学

Journal of Leukocyte Biology Pub Date : 2024-11-12 DOI: 10.1093/jleuko/qiae239

Darpan Saraswat, Isolde Gina Rojas, Rohitashw Kumar, Rui Li, Ornella Salvatori, Daniel Irimia, Mira Edgerton

{"title":"Neutrophil swarming is crucial for limiting oral mucosal infection by Candida albicans.","authors":"Darpan Saraswat, Isolde Gina Rojas, Rohitashw Kumar, Rui Li, Ornella Salvatori, Daniel Irimia, Mira Edgerton","doi":"10.1093/jleuko/qiae239","DOIUrl":"10.1093/jleuko/qiae239","url":null,"abstract":"Oral mucosal colonization by C. albicans (Ca) is benign in healthy people but progresses to deeper infection known as oropharyngeal candidiasis (OPC) that may become disseminated when combined with immunosuppression. Cortisone use and neutropenia are risk factors for invasive mucosal fungal infections, however the mechanisms are poorly understood. Here we identify in vivo neutrophil functional complexes known as swarms that are crucial for preventing Ca epithelial invasion. Anti-Ly6G antibody treatment impaired swarm formation and increased fungal infection depth confirming the role of neutrophil swarms in limiting Ca invasion. Neutrophil swarm function could be disrupted by administration of resolvins, and required leukotriene B4 receptor 1 (BLT1) expression so that administration of a leukotriene synthesis inhibitor reduced neutrophil swarm size permitting Ca invasion beyond the basement membrane. Cortisone treatment similarly reduced neutrophil swarming behavior and BLT1 expression and delayed expression of epithelial cytokines and chemokines. Thus, swarm structures have an important function in preventing deep invasion by C. albicans within the oral mucosa and represent a mechanism for increased disease severity under immune deficient clinical settings.","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142621847","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}

引用次数: 0