Journal of immunology最新文献_第9页

Functional role of Kv1.3 localization in chimeric antigen receptor T cells. Kv1.3定位在嵌合抗原受体T细胞中的功能作用。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-24 DOI: 10.1093/jimmun/vkaf199

Ghofrane Medyouni, Orsolya Vörös, György Panyi, Péter Hajdu

引用次数: 0

Establishment of a mouse model of Sjögren syndrome-related interstitial lung disease. Sjögren综合征相关性间质性肺疾病小鼠模型的建立。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-24 DOI: 10.1093/jimmun/vkaf211

Xiuping Liang, Yanhong Li, Deying Huang, Xueting Zhao, Yinlan Wu, Ronghui Liao, Tong Wu, Ziyi Tang, Chunyu Tan, Lu Cheng, Yubin Luo, Yi Liu

{"title":"Establishment of a mouse model of Sjögren syndrome-related interstitial lung disease.","authors":"Xiuping Liang, Yanhong Li, Deying Huang, Xueting Zhao, Yinlan Wu, Ronghui Liao, Tong Wu, Ziyi Tang, Chunyu Tan, Lu Cheng, Yubin Luo, Yi Liu","doi":"10.1093/jimmun/vkaf211","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf211","url":null,"abstract":"Sjögren syndrome-related interstitial lung disease (SS-ILD) is a severe complication associated with significant morbidity and mortality. Despite its clinical importance, the underlying pathogenesis remains poorly understood, and effective therapeutic strategies are limited. The development of a reliable animal model for SS-ILD is crucial for elucidating disease mechanisms and facilitating the discovery of novel treatments. In this study, we established a SS-ILD mouse model by administering 3 mg/kg bleomycin (BLM) via tracheal exposure to NOD/Ltj mice, a spontaneous model of Sjögren syndrome, with ICR mice serving as controls. The successful induction of Sjögren syndrome was confirmed through histopathology, and SSA/SSB ELISAs. Following BLM administration, lung inflammation and fibrosis were evaluated in ICR and NOD/Ltj mice by imaging, histopathology, and flow cytometry. Both ICR and NOD/Ltj mice developed lung inflammation and fibrosis after BLM exposure. However, NOD/Ltj mice exhibited a more pronounced immune response in the lung, characterized by increased infiltration of immune cells, including monocytes, monocyte-derived macrophages, dendritic cells, neutrophils, T cells, and B cells. This model successfully recapitulates key features of SS-ILD, including concurrent lymphocyte infiltration in the salivary glands and inflammation and fibrosis in the lungs. This study established a novel SS-ILD mouse model replicating human disease pathology, offering a valuable tool for investigating pathogenesis and advancing therapeutic development.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957024","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

RACK1 is required for normal B cell development and signaling but not RAG1 degradation. 正常的B细胞发育和信号传递需要RACK1，但RAG1降解不需要。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-24 DOI: 10.1093/jimmun/vkaf217

Victoria L Palmer, N Max Schabla, Vikas Kumar, Patrick C Swanson

{"title":"RACK1 is required for normal B cell development and signaling but not RAG1 degradation.","authors":"Victoria L Palmer, N Max Schabla, Vikas Kumar, Patrick C Swanson","doi":"10.1093/jimmun/vkaf217","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf217","url":null,"abstract":"V(D)J recombination is constrained by timely degradation of the RAG1 and RAG2 proteins through distinct mechanisms. Previously, we showed that full-length RAG1 stability is regulated by viral protein R binding protein (VprBP) through its association with an amino-terminal region in RAG1, but the mechanism remains unclear. As an unbiased approach to uncover potential cofactors involved in the process, we compared protein interactomes between RAG1/RAG2 complexes formed when the amino-terminal third of RAG1 was present or absent. These experiments identified RACK1 as preferentially associating with full-length RAG1. Because RACK1 is implicated in mediating protein degradation in other contexts, we evaluated how loss of RACK1 in B cells affects B cell development and V(D)J recombination. We find that conditional disruption of Rack1 expression in the B lineage in mice blocks B cell development at the pro-B cell stage and impairs V(D)J recombination after Igh DH-JH rearrangement. In this background, enforced Bcl2 expression does not significantly rescue B cell development but does enable the V(D)J recombination defect to be bypassed. However, the phenotype of these mice does not show the excessive Igk rearrangement, skewing toward Igλ+ B cells, or increased RAG1 protein levels observed when VprBP expression is similarly disrupted in B cells, arguing against RACK1 serving as a cofactor in RAG1 degradation. Further studies provide evidence that loss of RACK1 in primary B cells dysregulates cell cycle progression, apoptosis, proliferation, and signaling through MAPK and NF-κB pathways.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12380162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957051","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

Complement C3 deficiency inhibits osteoclast differentiation and prevents ovariectomy-induced osteoporosis. 补体C3缺乏抑制破骨细胞分化和预防卵巢切除术引起的骨质疏松症。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-22 DOI: 10.1093/jimmun/vkaf180

Adrita Guha, Arpita Prasad, Krishna Ashokkumar, Pradipta Pal, Arvind Sahu, Mohan R Wani, Girdhari Lal

{"title":"Complement C3 deficiency inhibits osteoclast differentiation and prevents ovariectomy-induced osteoporosis.","authors":"Adrita Guha, Arpita Prasad, Krishna Ashokkumar, Pradipta Pal, Arvind Sahu, Mohan R Wani, Girdhari Lal","doi":"10.1093/jimmun/vkaf180","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf180","url":null,"abstract":"The pathomechanistic role of the complement system is well recognized in various pathological conditions affecting bone tissues and the bone microenvironment, including rheumatoid arthritis, osteoarthritis, bone fractures, and periodontitis. The homeostasis of the bone is maintained by continuous remodeling, in which bone-resorbing or demineralizing osteoclast cells remove bone calcification, and osteoblast cells deposit new bone matrix. Major complement protein C3 is reported to control endochondral ossification, cartilage-to-bone transition, and longitudinal bone growth. The role of the complement protein C3 in differentiating multinucleated osteoclast cells (bone-resorbing cells) from osteoclast precursor cells (OCPs) and its contribution to long bone microarchitecture and strength are unclear. We demonstrated that C3 promotes the differentiation of osteoclasts and the formation of multinucleated osteoclasts from bone marrow-derived OCPs. C3-/- mice OCPs had reduced osteoclast-associated gene expression of TRAP (tartrate-resistant acid phosphatase), cathepsin K, calcitonin receptor, and RANK (receptor activator of nuclear factor κB) molecules compared with osteoclasts derived from wild-type (WT) OCPs. C3-/- mice had significantly increased bone mineral density and other bone parameters of the femur compared with WT mice. Furthermore, compared with WT mice, C3-/- mice were protected from ovariectomy-induced osteoporosis, characterized by significantly increased Foxp3+CD4+ T cells in the spleen and interleukin-10-producing B cells in both the spleen and the bone marrow. Intriguingly, C3 knockout mice exhibit reduced differentiation of functional osteoclast cells, which promotes a strong bone microarchitecture, suggesting that complement pathways may be explored as a therapeutic target in bone inflammatory diseases.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957048","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

In a model of parasite-mediated exhaustion, stem-like CD8 T cells differentiate into an unconventional intermediate effector memory subset. 在寄生虫介导的衰竭模型中，干细胞样CD8 T细胞分化为一种非常规的中间效应记忆亚群。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-22 DOI: 10.1093/jimmun/vkaf165

Magali M Moretto, Keer Chen, Christina Cox, Jie Chen, Imtiaz A Khan

{"title":"In a model of parasite-mediated exhaustion, stem-like CD8 T cells differentiate into an unconventional intermediate effector memory subset.","authors":"Magali M Moretto, Keer Chen, Christina Cox, Jie Chen, Imtiaz A Khan","doi":"10.1093/jimmun/vkaf165","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf165","url":null,"abstract":"CD8 T cell exhaustion has been reported in mice susceptible to Toxoplasma gondii infection. While the differentiation of CD8 exhausted subsets has been extensively reported, most of these studies have been conducted in chronic viral and cancer models. During chronic T. gondii infection, phenotypic and transcriptomic analyses of the polyclonal antigen-specific CD8 T cell response characterize 4 populations based on KLRG1 and CD62L expression. Pop1 (KLRG1+CD62Llo) bears the attributes of a terminal effector subset, and pop2 (KLRG1-CD62Llo) is similar to effector memory CD8 T cells. Akin to chronic viral infection and cancer systems, pop3 (KLRG1-CD62Lhi) exhibits the characteristics of stem-like progenitor CD8 T cells (high Tcf7, Slamf6, and Cxcr5 expression), whereas pop4 (KLRG1+CD62Lhi) closely resembles a transitory subset (elevated Tbx21, low Tcf1, and Tox expression). During chronic viral infection, the stem-like progenitor CD8 T cells transition into a terminally differentiated exhausted subset via an intermediate population. However, in our system, pop3 (KLRG1-CD62Lhi) generates pop4 (KLRG1+CD62Lhi), which does not convert into a conventional terminally differentiated exhausted subset but instead transitions into effector pop1 (KLRG1+CD62Llo). Notably, during the chronic phase of the infection, pop1 cannot retain its functionality, irrespective of its origin, which may hamper its ability to control reactivation. Our observations emphasize that the differentiation of exhausted CD8 T cells in non-viral infections, like chronic toxoplasmosis, follows a different pattern than established models and highlights the need to develop new immune strategies better tailored for a broad range of pathogens.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957062","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

Complement therapeutic factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections. 补体治疗因子H-IgG蛋白作为暴露前预防莱姆病感染的研究。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-22 DOI: 10.1093/jimmun/vkaf195

Connor W McKaig, Jill Malfetano, Y Tran, Xiuli Yang, Utpal Pal, Keith Wycoff, Yi-Pin Lin

{"title":"Complement therapeutic factor H-IgG proteins as pre-exposure prophylaxes against Lyme borreliae infections.","authors":"Connor W McKaig, Jill Malfetano, Y Tran, Xiuli Yang, Utpal Pal, Keith Wycoff, Yi-Pin Lin","doi":"10.1093/jimmun/vkaf195","DOIUrl":"10.1093/jimmun/vkaf195","url":null,"abstract":"Lyme disease (LD) is the most common vector-borne disease in the northern hemisphere and is caused by the bacteria Borrelia burgdorferi sensu lato (also known as Lyme borreliae) with no effective prevention available. Lyme borreliae evade complement killing, a critical arm of host immune defense, by producing outer surface proteins that bind to a host complement inhibitor, factor H (FH). These outer surface proteins include CspA and CspZ, which bind to the sixth and seventh short consensus repeats (SCR6-7) of FH and the OspE family of proteins (OspE), which bind to the nineteenth and twentieth SCR (SCR19-20). In this study, we produced 2 chimeric proteins, FH-Fc, containing the Fc region of immunoglobulin G (Fc) with SCR6-7 or SCR19-20. We found that both FH-Fc constructs killed B. burgdorferi via bacterial lysis and phagocytosis and reduced bacterial colonization and LD-associated joint inflammation in vivo. While SCR6-7-Fc displayed Lyme borreliae species-specific bacterial killing, SCR19-20-Fc versatilely eradicated all tested bacterial species/strains. This correlated with SCR6-7-Fc binding to select variants of CspA and CspZ, but SCR19-20-Fc binding to all tested OspE variants. Overall, we demonstrated the concept of using FH-Fc constructs to kill Lyme borreliae and defined underlying mechanisms, highlighting the potential of FH-Fc as a pre-exposure prophylaxis against LD infection.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12435995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957053","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

Optimized detection and inference of immune cell type names in single-cell RNA sequencing data. 单细胞RNA测序数据中免疫细胞类型名称的优化检测与推断。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-21 DOI: 10.1093/jimmun/vkaf183

Janyerkye Tulyeu, David Priest, James B Wing, Jonas Nørskov Søndergaard

引用次数: 0

MKLN1-dependent GID4/CTLH E3 ubiquitin ligase complex assemblies are required to support B-cell antibody diversification. mkln1依赖性GID4/CTLH E3泛素连接酶复合体是支持b细胞抗体多样化所必需的。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-20 DOI: 10.1093/jimmun/vkaf201

Philip Barbulescu, Matthew K Wong, Leon Baronian, Pengyu Wang, Abdulmateen Aderinto, Matthias Kneussel, Alberto Martin

{"title":"MKLN1-dependent GID4/CTLH E3 ubiquitin ligase complex assemblies are required to support B-cell antibody diversification.","authors":"Philip Barbulescu, Matthew K Wong, Leon Baronian, Pengyu Wang, Abdulmateen Aderinto, Matthias Kneussel, Alberto Martin","doi":"10.1093/jimmun/vkaf201","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf201","url":null,"abstract":"C-terminal to LisH (CTLH) E3 ubiquitin ligase complexes regulate a broad range of biological processes and forms separate supramolecular CTLH-MKLN1 and CTLH-WDR26 assemblies possessing distinct substrate specificities. Our previous work revealed that the CTLH complex utilizes the FAM72A substrate adaptor to ubiquitinate and degrade the uracil-DNA glycosylase 2 (UNG2) base excision repair factor. This outcome in B cells permits deoxyuridine mutations catalyzed by activation-induced cytidine deaminase (AID) to persist toward mutational outcomes and drive antibody diversification events. Here, we report that Mkln1-/- mice specifically lacking assembly of CTLH-MKLN1 complexes display reduced somatic hypermutation and class switch recombination frequencies due to increased UNG2, similar to Fam72a-/- mice. Strikingly, Mkln1-/- mice showed increased germinal center B cells and defects during B-cell development, a phenotype not observed in Fam72a-/- mice, suggesting that MKLN1 regulates proteins that are independent of FAM72A. Together, this work identifies that CTLH-MKLN1 ubiquitin E3 ligase complexes are critical in generating effective humoral immune responses and reveals distinctions between FAM72A-dependent and -independent CTLH complex modalities.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144956994","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 transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity. 转录因子BCL11B驱动NK细胞的细胞毒性和抗肿瘤活性。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-20 DOI: 10.1093/jimmun/vkaf179

Akhilesh Kumar, Bin Zhang, Andrew Baldys, Colin Fischer, Alexander Lenvik, Martin Felices, Zachary B Davis, Laura Bendzick, Anna J Weis, Yenan T Bryceson, Jeffrey S Miller, Frank Cichocki

{"title":"The transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity.","authors":"Akhilesh Kumar, Bin Zhang, Andrew Baldys, Colin Fischer, Alexander Lenvik, Martin Felices, Zachary B Davis, Laura Bendzick, Anna J Weis, Yenan T Bryceson, Jeffrey S Miller, Frank Cichocki","doi":"10.1093/jimmun/vkaf179","DOIUrl":"https://doi.org/10.1093/jimmun/vkaf179","url":null,"abstract":"Bcl11b is a zinc-finger transcription factor that is required for the differentiation of αβ T cells. A role for BCL11B in the regulation of human natural killer (NK) cell maturation has been inferred from patients with heterozygous mutations in BCL11B. However, mechanistic and functional studies are lacking due to the low efficiency of current transduction and transfection methods. Here, we developed a synthetic BCL11B mRNA with enhanced stability that could be transfected into primary NK cells at high frequencies. Introduction of BCL11B mRNA slowed NK cell proliferation while simultaneously driving maturation and acquisition of cytotoxic granule components. For in vitro and in vivo functional testing, we generated induced pluripotent stem cell (iPSC)-derived NK (iNK) cells with inducible BCL11B expression. These iNK cells mediated faster solid tumor cell killing and significantly better tumor control in vivo. Together, our findings support the notion that BCL11B is a key transcription factor in human NK cells and demonstrate that increased BCL11B expression can enhance NK cell immunotherapy.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144956989","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

TLR4al senses heme as a key damage/danger-associated molecular pattern to activate immune responses in lower vertebrates. TLR4al感知血红素是激活低等脊椎动物免疫反应的关键损伤/危险相关分子模式。

IF 3.4 3区医学

Journal of immunology Pub Date : 2025-08-19 DOI: 10.1093/jimmun/vkaf192

Ningxia Xiong, Maolin Lv, Jingjing Zhang, Yuezong Xu, Bo Tang, Chunrong Yang, Jianguo Su

{"title":"TLR4al senses heme as a key damage/danger-associated molecular pattern to activate immune responses in lower vertebrates.","authors":"Ningxia Xiong, Maolin Lv, Jingjing Zhang, Yuezong Xu, Bo Tang, Chunrong Yang, Jianguo Su","doi":"10.1093/jimmun/vkaf192","DOIUrl":"10.1093/jimmun/vkaf192","url":null,"abstract":"Toll-like receptor 4 (TLR4), a critical pattern recognition receptor, detects microbe- and damage/danger-associated molecular patterns to trigger immune responses in mammals. However, the functions and mechanisms remain largely unclear in lower vertebrates. This study systematically investigates the evolutionary divergence, subcellular localization and ligand of TLR4 in lower vertebrates by grass carp (Ctenopharyngodon idella) as a model species. TLR4 emerges and expands in a few teleosts but is absent in most fishes. We standardized the nomenclature of multiple TLR4 variants (3 or 4) in cyprinids. Tetrapods generally contain 1 TLR4. Astonishingly, CiTLR4ba, CiTLR4al, and CiTLR4bb localize to lysosomes but not cytomembrane like their mammalian counterparts, in which they recognize ligands that are engulfed into lysosomes. However, CiTLR4bc is soluble in cytoplasm due to the absence of signal peptide and transmembrane domain. In ligand recognition, CiTLR4 variants exhibit obvious heterogeneity. CiTLR4bc exhibits no binding activity to any of the tested ligands [lipopolysaccharide, peptidoglycan, bacterial dsDNA, polyinosinic-polycytidylic acid, heme]. Interestingly, both CiTLR4ba and CiTLR4bb bind polyinosinic-polycytidylic acid. Excitedly, CiTLR4al conservatively recognizes heme, a central damage/danger-associated molecular pattern (DAMP) released from damaged erythrocytes, in teleost and human. Further, 5 key high-affinity heme-binding sites (C113, H185, C295, H342, and C458) were identified in CiTLR4al. Each single key site mutation attenuates the heme-binding ability and downstream immune responses of CiTLR4al, supporting a multivalent heme-CiTLR4al interaction mechanism. The present study systematically elucidates the evolution of TLR4, as well as its complexity and conservation in vertebrates, offering direct evidence for the adaptive evolution of TLR4 in vertebrates. The results also contribute to the immune mechanism of hemolytic diseases.","PeriodicalId":16045,"journal":{"name":"Journal of immunology","volume":" ","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883009","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