Immunology最新文献

{"title":"Endogenous ERMAP Affects T-Cell Function in EAE Mice","authors":"Keke He,&nbsp;Kezhu Chen,&nbsp;Rong Hu,&nbsp;Tinghao Wen,&nbsp;Yuandi Li,&nbsp;Lu Xia,&nbsp;Li Xiao,&nbsp;Youbo Zhao,&nbsp;Dongbing Cui,&nbsp;Jie Gao,&nbsp;Lu Liu,&nbsp;Laijun Lai,&nbsp;Min Su","doi":"10.1111/imm.13910","DOIUrl":"10.1111/imm.13910","url":null,"abstract":"<div>\u0000 \u0000 <p>Multiple sclerosis (MS) is a central nervous system (CNS) autoimmune disease (AID) mediated by myelin-reactive CD4⁺ T cells. Experimental autoimmune encephalomyelitis (EAE) is a widely used animal model of human MS. Erythrocyte membrane-associated protein (ERMAP) is a novel erythrocyte-specific adhesion/receptor molecule associated with erythrocyte adhesion. We have previously characterised it as a novel inhibitory immune checkpoint molecule and demonstrated that recombinant ERMAP proteins ameliorate EAE; however, the specific mechanism of action of ERMAP and the effects of endogenous ERMAP on T-cell function are largely unknown. In this study, we investigate the role of endogenous ERMAP in T-cell and macrophage homeostasis and EAE development. We show here that erythrocyte membrane-associated protein (ERMAP) gene knockout (ERMAP^−/−) mice have increased numbers of T cells and pro-inflammatory M1 macrophages and enhanced T-cell activation, as compared to wild-type (ERMAP^+/+) mice. When induced to develop EAE, ERMAP^−/− mice have more severe EAE symptoms and pathology, which are related to increased numbers of T cells (especially Th1 and Th17 T cells) and M1 macrophages, enhanced activation of T cells, and increased generation of inflammatory cytokines, but decreased proportion of Th2 T cells, regulatory T cells (Tregs), and anti-inflammatory M2 macrophages. Global gene analysis by RNA-seq shows that signalling molecules in the peroxisome proliferator-activated receptor (PPAR) pathway are decreased in ERMAP^−/− mice. Our results suggest that endogenous ERMAP plays an important role in T-cell and macrophage homeostasis and EAE development.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"200-213"},"PeriodicalIF":4.9,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596998","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}

{"title":"Original Antigenic Sin in CD4+ T Cells","authors":"Mingran Zhang,&nbsp;Junling Ma,&nbsp;Meili Li","doi":"10.1111/imm.13916","DOIUrl":"10.1111/imm.13916","url":null,"abstract":"<div>\u0000 \u0000 <p>Original antigenic sin (OAS) describes the phenomenon in which prior exposure to an antigen weakens the adaptive antibody response to a subsequent heterologous infection. This phenomenon can diminish the effectiveness of immunity acquired through vaccination or previous infections. We demonstrate that OAS arises because CD4+ T cell proliferation and regulation signals are antigen-nonspecific. Rapidly responding memory CD4+ T cells trigger regulatory T cell (Tregs) responses, which prematurely suppress the naïve CD4+ T cell response, leading to a similar OAS effect in CD4+ T cells. This mechanism is illustrated through a mathematical model incorporating naïve and memory CD4+ T cell proliferation, interleukin-2 (IL-2), and Tregs. The model, calibrated with experimental data, employs numerical simulations to analyse how CD4+ T cell responses vary with the degree of cross-reactivity between memory CD4+ T cells and the antigen associated with the secondary infection. The findings indicate that the immune response is weakest at an intermediate level of cross-reactivity, a key characteristic of OAS. This mechanism may also explain OAS in antibody responses.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"165-179"},"PeriodicalIF":4.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585580","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}

{"title":"Computer Integrated Dominant Epitopes Evoke Protective Immune Response Against Streptococcus pneumoniae","authors":"Hitesh Harsukhbhai Chandpa,&nbsp;Shovan Naskar,&nbsp;Jairam Meena","doi":"10.1111/imm.13920","DOIUrl":"10.1111/imm.13920","url":null,"abstract":"<div>\u0000 \u0000 <p><i>Streptococcus pneumoniae</i> is a gram-positive bacterium responsible for various diseases like pneumonia, acute otitis media, sinusitis, meningitis and bacteraemia. These diseases cause a significant amount of morbidity and mortality. Although polysaccharide vaccines are available, the protection provided by these vaccines is serotype-dependent and not enough in sensitive populations like children and older people. Designing a subunit vaccine by using proteins that are responsible for the pathogenesis of diseases can provide better protection against bacterial infections. In this study, we present the design of a novel multi-epitope vaccine against <i>Streptococcus pneumoniae</i> using an immunoinformatic approach. More than 1170 epitopes were identified against B cells, cytotoxic T lymphocytes and helper T lymphocytes from more than 60 pneumococcal proteins. Epitopes were further screened, and potential epitopes were selected for vaccine development. Seven different vaccine combinations that harbour the 15 dominant B-cell, cytotoxic T cell and helper T cell epitopes were evaluated with linker and β-defensin adjuvant to finalise the best vaccine construct. Bioinformatics tools were used to analyse the construct's physicochemical properties, secondary and tertiary structures, allergenicity, antigenicity and immunogenicity. Docking studies with the TLR-4 receptor and molecular dynamics simulations indicated strong binding affinity and stability. In silico immune response simulations predicted robust IgG immune response generation and observed more than 200 000 IgG₁ + IgG₂ counts per mL. Similarly, cell-mediated immunity was also enhanced by the designed vaccine construct. The construct was codon-optimised and cloned in silico for expression in <i>Escherichia coli</i>. These findings suggest that the construct is a promising candidate for further experimental validation.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"180-199"},"PeriodicalIF":4.9,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585579","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}

{"title":"Cytotoxic Signature and IFN-γ Production Dominate CD4+ T-Cell Response During Human Toxoplasmosis","authors":"Priscilla Miranda Henriques,&nbsp;Gregório Guilherme Almeida,&nbsp;Inga Rimkute,&nbsp;Luara Isabela dos Santos,&nbsp;Thomas Liechti,&nbsp;Ana Paula Marino,&nbsp;Isabela Natália Pascoal Campos do Vale,&nbsp;Daniel Vitor Vasconcelos-Santos,&nbsp;Olindo Assis Martins-Filho,&nbsp;Ricardo Tostes Gazzinelli,&nbsp;Mario Roederer,&nbsp;Alan Sher,&nbsp;Andréa Teixeira-Carvalho,&nbsp;Dragana Jankovic,&nbsp;Lis Ribeiro do Valle Antonelli","doi":"10.1111/imm.13912","DOIUrl":"10.1111/imm.13912","url":null,"abstract":"<p><i>Toxoplasma gondii</i> is a highly versatile parasite that infects most warm-blooded animals and is a major cause of retinochoroiditis and uveitis in humans. The pathophysiology of these conditions remains poorly understood. Both parasite virulence and host inflammatory response contribute to the development of ocular disease. While CD4⁺ T cells play a critical role in host resistance to <i>Toxoplasma</i> infection, their kinetics and effector functions, as well as their contribution to the clinical outcome of the infection, including ocular involvement, remain poorly understood. To address this question, we investigated the immune response during acute and convalescent toxoplasmosis and stratified patients further based on the presence or absence of ocular disease. We found that <i>T. gondii</i> infection leads to decreased and increased proportions of central and effector memory CD4⁺ T cells, respectively. Applying unsupervised analysis, distinct CD4⁺ T-cell subsets were determined. Among 50 clusters, 10 produced cytotoxic proteins (granzyme B and perforin) and one produced cytokines upon antigen-specific stimulation. We observed that proportions of five CD4⁺ T-cell clusters out of 50 were different during acute disease between <i>T. gondii</i>-infected patients with and without ocular lesions. Interestingly, three of the five displayed a cytotoxic signature indicating their possible involvement in ocular immunopathology. Taken together, our results reveal that during <i>T. gondii</i> infection, CD4⁺ T cells not only develop a Th1 cytokine profile, but also acquire previously unappreciated cytotoxic capacity/function. These results, while underscoring the complexity of the CD4⁺ T-cell response to <i>T. gondii</i>, suggest that specific subsets may be involved in the development of pathology and provide possible targets for therapeutic intervention.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 2","pages":"151-164"},"PeriodicalIF":4.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541260","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}

{"title":"Ammonia-Induced Cell Death: A Novel Frontier to Enhance Cancer Immunotherapy","authors":"Urushi Rehman,&nbsp;Garima Gupta,&nbsp;Amirhossein Sahebkar,&nbsp;Prashant Kesharwani","doi":"10.1111/imm.13918","DOIUrl":"10.1111/imm.13918","url":null,"abstract":"<p>Cancer immunotherapy has revolutionized treatment paradigms, but its efficacy is often curtailed by T-cell exhaustion and the suppressive tumour microenvironment. Recent studies reveal a novel mechanism of T-cell demise termed ammonia-induced cell death (AICD), which significantly impacts effector CD8+ T-cell survival and function. This phenomenon arises from metabolic reprogramming during immune activation, wherein heightened glutamine metabolism leads to the accumulation of toxic ammonia levels. Ammonia damages lysosomes and mitochondria, disrupting cell balance and causing apoptosis. These insights provide a unique metabolic perspective on T-cell attrition, underscoring the critical interplay between metabolic byproducts and immune regulation. Targeting AICD offers promising therapeutic avenues to bolster immunotherapy. Strategies such as inhibiting ammonia transport, enhancing autophagic pathways and employing ammonia scavengers may extend T-cell longevity and improve antitumor efficacy. Moreover, integrating ammonia modulation with established immunotherapies, including immune checkpoint inhibitors and chimeric antigen receptor (CAR) T-cell therapy, could yield synergistic benefits. Addressing this metabolic bottleneck is particularly compelling in immune ‘cold’ tumours resistant to conventional therapies. However, further research is essential to refine these interventions, evaluate safety profiles and explore broader applications across cancer types. Ammonia metabolism thus represents a transformative frontier in advancing cancer immunotherapy and precision oncology.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"16-20"},"PeriodicalIF":4.9,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13918","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541114","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}

{"title":"Successful Treatment of Chronic Rhinosinusitis With Nasal Polyps (CRSwNP) With Tezepelumab: A Case Report.","authors":"Mattia Cristallo, Mirco Filieri, Federico Spataro, Loredana Muolo, Eustachio Nettis, Attilio Di Girolamo","doi":"10.1111/imm.13915","DOIUrl":"https://doi.org/10.1111/imm.13915","url":null,"abstract":"","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537083","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}

{"title":"Diagnostic Significance of Metagenomic Next-Generation Sequencing in Immunocompromised Patients With Suspected Pulmonary Infection","authors":"Xi Zheng,&nbsp;Wei Zou,&nbsp;Shumei Zou,&nbsp;Jia Ye,&nbsp;Zhenming Bao,&nbsp;Yingfang Song","doi":"10.1111/imm.13911","DOIUrl":"10.1111/imm.13911","url":null,"abstract":"<p>Immunocompromised hosts are highly vulnerable to lung infections, but the efficacy of traditional diagnosis is unsatisfactory. Metagenomic next-generation sequencing (mNGS) has high throughput and broad coverage. Its value in different types of immunocompromised patients has yet to be fully explored. Therefore, the study aims to evaluate the value of mNGS in immunocompromised patients. Clinical data from immunocompromised patients with suspected pulmonary infection (PI) (September 2018–2021) were retrospectively analysed. Patients were categorised into PI (87 cases) and non-pulmonary infection (NPI, 14 cases) groups. The diagnostic performance between mNGS and conventional microbiological tests (CMTs) was compared. Subgroup analyses were also conducted based on whether the patients received organ transplantation, including the comparison of the diagnostic performance of mNGS and culture and the spectrum of characteristics among them. mNGS demonstrated significantly elevated diagnostic sensitivity (<i>p</i> &lt; 0.001) over traditional methods, with a pronounced advantage in identifying mixed PIs (<i>p</i> &lt; 0.05). Among immunocompromised cohorts, mNGS outperformed cultures, showing higher positivity rates in both organ transplant (<i>p</i> &lt; 0.001) and non-transplant patients (<i>p</i> &lt; 0.001). Mixed infections, predominantly bacterial–fungal, were more prevalent in transplant recipients with reduced lymphocytes and CD4⁺ T cells. Pathogen profiles differed, with <i>Pneumocystis jirovecii</i>, <i>Cytomegalovirus</i>, and \u0000 <i>Pseudomonas aeruginosa</i>\u0000 predominating in organ transplant recipients, and <i>P. jirovecii</i>, \u0000 <i>P. aeruginosa</i>\u0000 , \u0000 <i>Streptococcus pneumoniae</i>\u0000 and <i>Streptococcus pallidum</i> in non-transplant individuals. mNGS is valuable in diagnosing PI and mixed infections in immunocompromised patients, which may be particularly suitable for identifying mixed infections in patients with organ transplants and low lymphocyte and CD4⁺ T lymphocyte counts.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"112-122"},"PeriodicalIF":4.9,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13911","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482760","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}

{"title":"Comparative Analysis of HMC3 and C20 Microglial Cell Lines Reveals Differential Myeloid Characteristics and Responses to Immune Stimuli","authors":"Bavani Gunasegaran,&nbsp;Shivani Krishnamurthy,&nbsp;Sharron S. Chow,&nbsp;Millijoy D. Villanueva,&nbsp;Anna Guller,&nbsp;Seong Beom Ahn,&nbsp;Benjamin Heng","doi":"10.1111/imm.13900","DOIUrl":"10.1111/imm.13900","url":null,"abstract":"<p>Microglia are the primary resident immune cells of the central nervous system (CNS) that respond to injury and infections. Being critical to CNS homeostasis, microglia also have been shown to contribute to neurodegenerative diseases and brain cancer. Hence, microglia are regarded as a potential therapeutic target in CNS diseases, resulting in an increased demand for reliable in vitro models. Two human microglia cell lines (HMC3 and C20) are being used in multiple in vitro studies, however, the knowledge of their biological and immunological characteristics remains limited. Our aim was to identify and compare the biological changes in these immortalised immune cells under normal physiological and immunologically challenged conditions. Using high-resolution quantitative mass spectrometry, we have examined in-depth proteomic profiles of non-stimulated and LPS or IFN-γ challenged HMC3 and C20 cells. Our findings reveal that HMC3 cells responded to both treatments through upregulation of immune, metabolic, and antiviral pathways, while C20 cells showed a response associated with mitochondrial and immune activities. Additionally, the secretome analysis demonstrated that both cell lines release IL-6 in response to LPS, while IFN-γ treatment resulted in altered kynurenine pathway activity, highlighting distinct immune and metabolic adaptations.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"84-102"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/imm.13900","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440705","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}

{"title":"Lineage Tracking Dissects the Fate of Neonatal iNKT Cells Later in Life","authors":"Jun Liu,&nbsp;Biao Yang,&nbsp;Danchen Hu,&nbsp;Ning Yuan,&nbsp;Wenhua Li,&nbsp;Zhao Feng,&nbsp;Yanhong Su,&nbsp;Dan Zhang,&nbsp;Xiaofeng Yang,&nbsp;Baojun Zhang","doi":"10.1111/imm.13909","DOIUrl":"10.1111/imm.13909","url":null,"abstract":"<div>\u0000 \u0000 <p>Invariant natural killer T (iNKT) cells in peripheral tissues are from different waves ranged from foetal, neonatal to adult ages. However, it is unclear how iNKT cells from different ages maintain in the periphery and what are their functionality. We found that in adult mice, neonate tracked-iNKT (NT-iNKT) cells are present in spleen, bone marrow, liver and lung, with a predominantly accumulation in the kidney. The NT-iNKT cells in the kidney are almost iNKT1 cells and express tissue-resident marker CD69. These cells also exhibit higher level of CD122 and possess a stronger proliferative capacity compared to adult tracked-iNKT (AT-iNKT) cells. Furthermore, we found that NT-iNKT cells potentially secrete more IFN-γ than AT-iNKT cells in vitro and in vivo (a-GalCer immunisation). Overall, our study sheds light on the peripheral behaviour and functionality of NT- and AT-iNKT cells, highlighting the potential role of NT-iNKT cells in the kidney during immune response.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"103-111"},"PeriodicalIF":4.9,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143432793","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}

{"title":"Icariin Induces Chondrocyte Degeneration via Activation of the NF-κB Signalling Pathway and Reduces the Inflammation Factor Expression Induced by Lipopolysaccharide","authors":"Tianjun Zhai,&nbsp;Jie Wang,&nbsp;Yeping Chen,&nbsp;Jianqing Su,&nbsp;Wei Feng","doi":"10.1111/imm.13906","DOIUrl":"10.1111/imm.13906","url":null,"abstract":"<div>\u0000 \u0000 <p>To investigate the effect of icariin on chondrocytes by activating the nuclear factor kappa-B (NF-κB) signalling pathway and the mechanism of icariin in inducing chondrocytes degeneration. Chondrocytes were cultured in vitro and treated with icariin at concentrations of 0, 0.01, 0.1, 10 and 20 μm. Cell proliferation was evaluated by cell counting kit-8 (CCK8) method, apoptosis was detected by TUNEL method and the expression of NF-κB was detected by Western blotting (WB) and RT-PCR. The nuclear localization of NF-κB p65 protein was observed by immunofluorescence staining. Lipopolysaccharide (LPS) was used to establish the inflammatory model, and WB and RT-PCR were used to detect the expression levels of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6). After treatment with icariin, the proliferation ability of chondrocytes was markedly enhanced, and the apoptosis rate (AR) was markedly decreased (<i>p &lt;</i> 0.05). In addition, icariin could inhibit the nuclear translocation of NF-κB p65 protein, promote the gene expression of Collagen II (Col-II) and Aggrecan in chondrocytes, and reduce the expression of NF-κB. Moreover, icariin markedly reduced the expression of IL-6 and TNF-α in LPS-induced inflammation (<i>p &lt;</i> 0.05). Icariin can enhance chondrocyte proliferation, promote phenotypic gene expression by inhibiting the NF-κB signal transduction pathways, thus suppressing the chondrocyte degeneration, and can reduce the inflammation factor expression induced by LPS.</p>\u0000 </div>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":"175 1","pages":"76-83"},"PeriodicalIF":4.9,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414073","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}