Journal of immunology最新文献_第4页

Maternal Helminth Infection Causes Dysfunctional B Cell Development in Male Offspring. 母体螺旋体感染导致雄性后代 B 细胞发育失调

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-15 DOI: 10.4049/jimmunol.2400158

Lisa C Gibbs, Juan M Oviedo, Bartholomew N Ondigo, Keke C Fairfax

{"title":"Maternal Helminth Infection Causes Dysfunctional B Cell Development in Male Offspring.","authors":"Lisa C Gibbs, Juan M Oviedo, Bartholomew N Ondigo, Keke C Fairfax","doi":"10.4049/jimmunol.2400158","DOIUrl":"10.4049/jimmunol.2400158","url":null,"abstract":"Infections during pregnancy are known to trigger alterations in offspring immunity, often leading to increased disease susceptibility. Maternal helminth infections correlate with lower Ab titers to certain childhood immunizations and putative decreased vaccine efficacy. The mechanisms that underlie how maternal infection blunts offspring humoral responses are unclear. Using our murine model of maternal schistosomiasis, we found that maternal helminth infection decreases the germinal center response of all offspring to tetanus immunization. However, only male offspring have defects in memory B cell and long-lived plasma cell generation. We found this sex-specific aberration begins during B cell development within the bone marrow via alteration of the IL-7 niche and persists throughout antigenic activation in the germinal center in the periphery. Critically, these defects in males are cell intrinsic, persisting following adoptive transfer to control male pups. Together, these data show that maternal infections can alter both the bone marrow microenvironment and the development of B lymphocytes in a sex-specific manner. This study correlates maternal infection induced defects in early life B cell development with ineffective Ab responses after vaccination.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11537230/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142055797","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

An Integrated Signaling Threshold Initiates IgG Response toward Virus-like Immunogens. 综合信号阈值启动 IgG 对病毒样免疫原的反应

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-15 DOI: 10.4049/jimmunol.2400101

Wei-Yun Wholey, Alexander R Meyer, Sekou-Tidiane Yoda, James L Mueller, Raisa Mathenge, Bryce Chackerian, Julie Zikherman, Wei Cheng

{"title":"An Integrated Signaling Threshold Initiates IgG Response toward Virus-like Immunogens.","authors":"Wei-Yun Wholey, Alexander R Meyer, Sekou-Tidiane Yoda, James L Mueller, Raisa Mathenge, Bryce Chackerian, Julie Zikherman, Wei Cheng","doi":"10.4049/jimmunol.2400101","DOIUrl":"10.4049/jimmunol.2400101","url":null,"abstract":"Class-switched neutralizing Ab (nAb) production is rapidly induced upon many viral infections. However, due to the presence of multiple components in virions, the precise biochemical and biophysical signals from viral infections that initiate nAb responses remain inadequately defined. Using a reductionist system of synthetic virus-like structures, in this study, we show that a foreign protein on a virion-sized liposome can serve as a stand-alone danger signal to initiate class-switched nAb responses without T cell help or TLR but requires CD19. Introduction of internal nucleic acids (iNAs) obviates the need for CD19, lowers the epitope density (ED) required to elicit the Ab response, and transforms these structures into highly potent immunogens that rival conventional virus-like particles in their ability to elicit strong Ag-specific IgG. As early as day 5 after immunization, structures harboring iNAs and decorated with just a few molecules of surface Ag at doses as low as 100 ng induced all IgG subclasses of Ab in mice and reproduced the IgG2a/2c restriction that is long observed in live viral infections. These findings reveal a shared mechanism for the nAb response in mice. High ED is capable but not necessary for driving Ab secretion. Instead, even a few molecules of surface Ag, when combined with nucleic acids within these structures, can trigger strong IgG production. As a result, the signaling threshold for induction of IgG in individual B cells is set by dual signals originating from both ED on the surface and the presence of iNAs within viral particulate immunogens.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142108109","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

IDO2 Drives Autoantibody Production and Joint Inflammation in a Preclinical Model of Arthritis by Repressing Runx1 Function in B Cells. IDO2 通过抑制 B 细胞中 Runx1 的功能，驱动关节炎临床前模型中自身抗体的产生和关节炎症。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-14 DOI: 10.4049/jimmunol.2400445

Weidan Peng, Lauren M F Merlo, Samantha Grabler, James D Montgomery, Laura Mandik-Nayak

{"title":"IDO2 Drives Autoantibody Production and Joint Inflammation in a Preclinical Model of Arthritis by Repressing Runx1 Function in B Cells.","authors":"Weidan Peng, Lauren M F Merlo, Samantha Grabler, James D Montgomery, Laura Mandik-Nayak","doi":"10.4049/jimmunol.2400445","DOIUrl":"https://doi.org/10.4049/jimmunol.2400445","url":null,"abstract":"The immunomodulatory enzyme IDO2 is an essential mediator of autoantibody production and joint inflammation in preclinical models of autoimmune arthritis. Although originally identified as a tryptophan-catabolizing enzyme, we recently discovered a previously unknown nonenzymatic pathway is essential for the proarthritic function of IDO2. We subsequently identified Runx1 (Runt-related transcription factor 1) as a potential component of the nonenzymatic pathway IDO2 uses to drive arthritis. In this study, we find that IDO2 directly binds Runx1 and inhibits its localization to the nucleus, implicating Runx1 as a downstream component of IDO2 function. To directly test whether Runx1 mediates the downstream pathway driving B cell activation in arthritis, we bred B cell conditional Runx1-deficient (CD19cre Runx1flox/flox) mice onto the KRN.g7 arthritis model in the presence or absence of IDO2. Runx1 loss did not affect arthritis in the presence of IDO2; however, deleting Runx1 reversed the antiarthritic effect of IDO2 loss in this model. Further studies demonstrated that the IDO2-Runx1 interaction could be blocked with a therapeutic anti-IDO2 mAb in vitro and that Runx1 was required for IDO2 Ig's therapeutic effect in vivo. Taken together, these data demonstrate that IDO2 mediates autoantibody production and joint inflammation by acting as a repressor of Runx1 function in B cells and implicate therapeutic targeting of IDO2-Runx1 binding as a strategy to inhibit autoimmune arthritis and other autoantibody-mediated diseases.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142467518","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

Podosome Nucleation Is Facilitated by Multivalent Interactions between Syk and ITAM-containing Membrane Complexes. Syk与含ITAM的膜复合物之间的多价相互作用促进了荚膜体的形成

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400031

Sina Ghasempour, Aleixo M Muise, Spencer A Freeman

{"title":"Podosome Nucleation Is Facilitated by Multivalent Interactions between Syk and ITAM-containing Membrane Complexes.","authors":"Sina Ghasempour, Aleixo M Muise, Spencer A Freeman","doi":"10.4049/jimmunol.2400031","DOIUrl":"10.4049/jimmunol.2400031","url":null,"abstract":"Immune cells survey their microenvironment by forming dynamic cellular protrusions that enable chemotaxis, contacts with other cells, and phagocytosis. Podosomes are a unique type of protrusion structured by an adhesive ring of active integrins that surround an F-actin-rich core harboring degradative proteases. Although the features of podosomes, once-established, have been well defined, the steps that lead to podosome formation remain poorly understood by comparison. In this study, we report that spleen tyrosine kinase (Syk) is a critical regulator of podosome formation. Deletion of Syk or targeting its kinase activity eliminated the ability for murine macrophages to form podosomes. We found that the kinase activity of Syk was important for the phosphorylation of its substrates, HS1 and Pyk2, both of which regulate podosome formation. Additionally, before podosomes form, we report that the tandem Src homology 2 domains of Syk afforded multivalent clustering of ITAM-containing adaptors that associated with integrins to structure platforms that initiate podosomes. We therefore propose that Syk has a dual role in regulating podosomes: first, by facilitating the assembly of multivalent signaling hubs that nucleate their formation and second, by sustaining tyrosine kinase activity of the podosomes once they form against their substrates. In cells expressing recently identified gain-of-function variants of SYK, podosomes were dysregulated. These results implicate SYK in the (patho)physiological functions of podosomes in macrophages.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11404668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975852","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

Gpx4 Regulates Invariant NKT Cell Homeostasis and Function by Preventing Lipid Peroxidation and Ferroptosis. Gpx4 通过防止脂质过氧化和铁氧化调节不变 NKT 细胞的稳态和功能

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400246

Sophia P M Sok, Kaitlyn Pipkin, Narcis I Popescu, Megan Reidy, Bin Li, Holly Van Remmen, Mike Kinter, Xiao-Hong Sun, Zhichao Fan, Meng Zhao

{"title":"Gpx4 Regulates Invariant NKT Cell Homeostasis and Function by Preventing Lipid Peroxidation and Ferroptosis.","authors":"Sophia P M Sok, Kaitlyn Pipkin, Narcis I Popescu, Megan Reidy, Bin Li, Holly Van Remmen, Mike Kinter, Xiao-Hong Sun, Zhichao Fan, Meng Zhao","doi":"10.4049/jimmunol.2400246","DOIUrl":"10.4049/jimmunol.2400246","url":null,"abstract":"Invariant NKT (iNKT) cells are a group of innate-like T cells that plays important roles in immune homeostasis and activation. We found that iNKT cells, compared with CD4+ T cells, have significantly higher levels of lipid peroxidation in both mice and humans. Proteomic analysis also demonstrated that iNKT cells express higher levels of phospholipid hydroperoxidase glutathione peroxidase 4 (Gpx4), a major antioxidant enzyme that reduces lipid peroxidation and prevents ferroptosis. T cell-specific deletion of Gpx4 reduces iNKT cell population, most prominently the IFN-γ-producing NKT1 subset. RNA-sequencing analysis revealed that IFN-γ signaling, cell cycle regulation, and mitochondrial function are perturbed by Gpx4 deletion in iNKT cells. Consistently, we detected impaired cytokine production, elevated cell proliferation and cell death, and accumulation of lipid peroxides and mitochondrial reactive oxygen species in Gpx4 knockout iNKT cells. Ferroptosis inhibitors, iron chelators, vitamin E, and vitamin K2 can prevent ferroptosis induced by Gpx4 deficiency in iNKT cells and ameliorate the impaired function of iNKT cells due to Gpx4 inhibition. Last, vitamin E rescues iNKT cell population in Gpx4 knockout mice. Altogether, our findings reveal the critical role of Gpx4 in regulating iNKT cell homeostasis and function, through controlling lipid peroxidation and ferroptosis.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11408103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142000103","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

Cutting Edge: Retinoic Acid Promotes Brain-homing of CD8+ T Cells during Congenital Cytomegalovirus Infection. 前沿：视黄酸在先天性巨细胞病毒感染过程中促进 CD8+ T 细胞的脑归属。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400150

Zachary T Hilt, Wisler Charles, Taha Ali, Casey V Smith, Shide Zhang, Samantha P Wesnak, Norah L Smith, Brian D Rudd

引用次数: 0

Cell-surface Milieu Remodeling in Human Dendritic Cell Activation. 人类树突状细胞活化过程中的细胞表面环境重塑

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400089

Namrata D Udeshi, Charles Xu, Zuzhi Jiang, Shihong Max Gao, Qian Yin, Wei Luo, Steven A Carr, Mark M Davis, Jiefu Li

{"title":"Cell-surface Milieu Remodeling in Human Dendritic Cell Activation.","authors":"Namrata D Udeshi, Charles Xu, Zuzhi Jiang, Shihong Max Gao, Qian Yin, Wei Luo, Steven A Carr, Mark M Davis, Jiefu Li","doi":"10.4049/jimmunol.2400089","DOIUrl":"10.4049/jimmunol.2400089","url":null,"abstract":"Dendritic cells (DCs) are specialized sentinel and APCs coordinating innate and adaptive immunity. Through proteins on their cell surface, DCs sense changes in the environment, internalize pathogens, present processed Ags, and communicate with other immune cells. By combining chemical labeling and quantitative mass spectrometry, we systematically profiled and compared the cell-surface proteomes of human primary conventional DCs (cDCs) in their resting and activated states. TLR activation by a lipopeptide globally reshaped the cell-surface proteome of cDCs, with >100 proteins upregulated or downregulated. By simultaneously elevating positive regulators and reducing inhibitory signals across multiple protein families, the remodeling creates a cell-surface milieu promoting immune responses. Still, cDCs maintain the stimulatory-to-inhibitory balance by leveraging a distinct set of inhibitory molecules. This analysis thus uncovers the molecular complexity and plasticity of the cDC cell surface and provides a roadmap for understanding cDC activation and signaling.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11408084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916926","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

TLR3/TRIF and MAVS Signaling Is Essential in Regulating Mucosal T Cell Responses during Rotavirus Infection. 轮状病毒感染期间，TLR3/TRIF 和 MAVS 信号在调控黏膜 T 细胞反应中至关重要。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2300867

Rong-Rong Zhang, Xue-Yao Yang, Yong-Lei Yang, Tian-Kui Guo, Jing-Shu Huang, Ying-Shi Yang, Chun-Wei Shi, Gui-Lian Yang, Hai-Bin Huang, Jian-Zhong Wang, Yan-Long Jiang, Xin Cao, Nan Wang, Yan Zeng, Wen-Tao Yang, Chun-Feng Wang

{"title":"TLR3/TRIF and MAVS Signaling Is Essential in Regulating Mucosal T Cell Responses during Rotavirus Infection.","authors":"Rong-Rong Zhang, Xue-Yao Yang, Yong-Lei Yang, Tian-Kui Guo, Jing-Shu Huang, Ying-Shi Yang, Chun-Wei Shi, Gui-Lian Yang, Hai-Bin Huang, Jian-Zhong Wang, Yan-Long Jiang, Xin Cao, Nan Wang, Yan Zeng, Wen-Tao Yang, Chun-Feng Wang","doi":"10.4049/jimmunol.2300867","DOIUrl":"10.4049/jimmunol.2300867","url":null,"abstract":"The functions of the natural dsRNA sensors TLR3 (TRIF) and RIG-I (MAVS) are crucial during viral challenge and have not been accurately clarified in adaptive immune responses to rotavirus (RV) infection. In this study, we found that RV infection caused severe pathological damage to the small intestine of TLR3-/- and TRIF-/- mice. Our data found that dendritic cells from TLR3-/- and TRIF-/- mice had impaired Ag presentation to the RV and attenuated initiation of T cells upon viral infection. These attenuated functions resulted in impaired CD4+ T and CD8+ T function in mice lacking TLR3-TRIF signaling postinfection. Additionally, attenuated proliferative capacity of T cells from TLR3-/- and TRIF-/- mice was observed. Subsequently, we observed a significant reduction in the absolute number of memory T cells in the spleen and mesenteric lymph node (MLN) of TRIF-/- recipient mice following RV infection in a bone marrow chimeric model. Furthermore, there was reduced migration of type 2 classical dendritic cells from the intestine to MLNs after RV infection in TLR3-/- and TRIF-/- mice. Notably, RV infection resulted in attenuated killing of spleen and MLN tissues in TRIF-/- and MAVS-/- mice. Finally, we demonstrated that RV infection promoted apoptosis of CD8+ T cells in TRIF-/- and TLR3-/-MAVS-/- mice. Taken together, our findings highlight an important mechanism of TLR3 signaling through TRIF in mucosal T cell responses to RV and lay the foundation for the development of a novel vaccine.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080570","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

Late-life Attenuation of Cytomegalovirus-mediated CD8 T Cell Memory Inflation: Shrinking of the Cytomegalovirus Latency Niche. 晚期巨细胞病毒介导的 CD8 T 细胞记忆性炎症衰减：巨细胞病毒潜伏龛缩小。

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400113

Christopher P Coplen, Sandip Ashok Sonar, Janko Ž Nikolich

引用次数: 0

Glucocorticoids Suppress NF-κB-Mediated Neutrophil Control of Aspergillus fumigatus Hyphal Growth. 糖皮质激素抑制 NF-κB 介导的中性粒细胞对曲霉菌茎突生长的控制作用

IF 3.6 3区医学

Journal of immunology Pub Date : 2024-10-01 DOI: 10.4049/jimmunol.2400021

Savini U Thrikawala, Molly H Anderson, Emily E Rosowski

{"title":"Glucocorticoids Suppress NF-κB-Mediated Neutrophil Control of Aspergillus fumigatus Hyphal Growth.","authors":"Savini U Thrikawala, Molly H Anderson, Emily E Rosowski","doi":"10.4049/jimmunol.2400021","DOIUrl":"10.4049/jimmunol.2400021","url":null,"abstract":"Glucocorticoids are a major class of therapeutic anti-inflammatory and immunosuppressive drugs prescribed to patients with inflammatory diseases, to avoid transplant rejection, and as part of cancer chemotherapy. However, exposure to these drugs increases the risk of opportunistic infections such as with the fungus Aspergillus fumigatus, which causes mortality in >50% of infected patients. The mechanisms by which glucocorticoids increase susceptibility to A. fumigatus are poorly understood. In this article, we used a zebrafish larva Aspergillus infection model to identify innate immune mechanisms altered by glucocorticoid treatment. Infected larvae exposed to dexamethasone succumb to infection at a significantly higher rate than control larvae. However, both macrophages and neutrophils are still recruited to the site of infection, and dexamethasone treatment does not significantly affect fungal spore killing. Instead, the primary effect of dexamethasone manifests later in infection with treated larvae exhibiting increased invasive hyphal growth. In line with this, dexamethasone predominantly inhibits neutrophil function rather than macrophage function. Dexamethasone-induced mortality also depends on the glucocorticoid receptor. Dexamethasone partially suppresses NF-κB activation at the infection site by inducing the transcription of IκB via the glucocorticoid receptor. Independent CRISPR/Cas9 targeting of IKKγ to prevent NF-κB activation also increases invasive A. fumigatus growth and larval mortality. However, dexamethasone treatment of IKKγ crispant larvae further increases invasive hyphal growth and host mortality, suggesting that dexamethasone may suppress other pathways in addition to NF-κB to promote host susceptibility. Collectively, we find that dexamethasone acts through the glucocorticoid receptor to suppress NF-κB-mediated neutrophil control of A. fumigatus hyphae in zebrafish larvae.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11408098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142043949","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