Journal of autoimmunity最新文献

{"title":"Effect of Epstein-Barr Virus infection on gene regulation in immune cells of patients with Immune-Mediated Diseases","authors":"Yuko Akutsu ,&nbsp;Mineto Ota ,&nbsp;Takahiro Itamiya ,&nbsp;Masaaki Mori ,&nbsp;Tomohiro Morio ,&nbsp;Kazuhiko Yamamoto ,&nbsp;Tomohisa Okamura ,&nbsp;Keishi Fujio","doi":"10.1016/j.jaut.2024.103355","DOIUrl":"10.1016/j.jaut.2024.103355","url":null,"abstract":"<div><div>It has been known that Epstein-Barr virus (EBV) can latently infect immune cells after the initial infection, and epidemiological studies have suggested its association with the onset of immune-mediated diseases (IMDs). However, the specific impact of EBV infection on IMDs pathology remains unclear. We quantified EBV load of B cell subsets (Naïve B cells, Unswitched memory B cells, Switched memory B cells, Double negative B cells, and Plasmablasts) in IMD patients as well as healthy control (HC) using bulk RNA sequencing data of 504 donors. The EBV load was clearly higher in IMD patients compared to HC. Furthermore, the wide range of EBV load in this dataset enabled us to assess the impact of EBV load on gene regulation. We found many examples of expression quantitative trait loci (eQTL) whose effects were associated with EBV load. Expression QTLs that exhibited larger effects with increasing EBV load were significantly overlapped with binding sites of transcription factors derived from the EBV genome. These EBV load-associated eQTLs exhibited high enrichment of systemic lupus erythematosus (SLE) GWAS signals, suggesting the mechanical link of EBV infection and the onset of the disease via gene regulation. These findings provide the first evidence of the influence of EBV infection on gene regulation in human primary cells and its association with the SLE onset and/or progression.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"150 ","pages":"Article 103355"},"PeriodicalIF":7.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142949502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in chimeric antigen receptor T cell therapy for autoimmune and autoinflammatory diseases and their complications","authors":"Liuting Zeng ,&nbsp;Yan Li ,&nbsp;Wang Xiang ,&nbsp;Wei Xiao ,&nbsp;Zhiyong Long ,&nbsp;Lingyun Sun","doi":"10.1016/j.jaut.2024.103350","DOIUrl":"10.1016/j.jaut.2024.103350","url":null,"abstract":"<div><div>Chimeric antigen receptor T (CAR-T) cells are genetically engineered T cells expressing transmembrane chimeric antigen receptors with specific targeting abilities. As an emerging immunotherapy, the use of CAR-T cells has made significant breakthroughs in cancer treatment, particularly for hematological malignancies. The success of CAR-T cell therapy in blood cancers highlights its potential for other conditions in which the clearance of pathological cells is therapeutic, such as liver diseases, infectious diseases, heart failure, and diabetes. Given the limitations of current therapies for autoimmune diseases, researchers have actively explored the potential therapeutic value of CAR-T cells and their derivatives in the field of autoimmune diseases. This review focuses on the research progress and current challenges of CAR-T cells in autoimmune diseases with the aim of providing a theoretical basis for the precise treatment of autoimmune diseases. In the future, CAR-T cells may present new therapeutic modalities and ultimately provide hope for patients with autoimmune diseases.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"150 ","pages":"Article 103350"},"PeriodicalIF":7.9,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating T cells in sarcoidosis have an aberrantly activated phenotype that correlates with disease outcome","authors":"Jelle R. Miedema ,&nbsp;Lieke J. de Jong ,&nbsp;Denise van Uden ,&nbsp;Ingrid M. Bergen ,&nbsp;Mirjam Kool ,&nbsp;Caroline E. Broos ,&nbsp;Vivienne Kahlmann ,&nbsp;Marlies S. Wijsenbeek ,&nbsp;Rudi W. Hendriks ,&nbsp;Odilia B.J. Corneth","doi":"10.1016/j.jaut.2023.103120","DOIUrl":"10.1016/j.jaut.2023.103120","url":null,"abstract":"<div><h3>Rationale</h3><div>Disease course in sarcoidosis is highly variable. Bronchoalveolar lavage fluid and mediastinal lymph nodes show accumulation of activated T cells with a T-helper (Th)17.1 signature, which correlates with non-resolving sarcoidosis. We hypothesize that the peripheral blood (PB) T cell phenotype may correlate with outcome.</div></div><div><h3>Objectives</h3><div>To compare frequencies, phenotypes and function of circulating T cell populations in sarcoidosis patients with healthy controls (HCs) and correlate these parameters with outcome.</div></div><div><h3>Methods</h3><div>We used multi-color flow cytometry to quantify activation marker expression on PB T cell subsets in treatment-naïve patients and HCs. The disease course was determined after 2-year follow-up. Cytokine production was measured after T cell stimulation <em>in vitro.</em></div></div><div><h3>Measurements and main results</h3><div>We observed significant differences between patients and HCs in several T cell populations, including CD8⁺ and CD4⁺ T cells, Th1/Th17 subsets, CD4⁺ T memory stem cells, regulatory T cells (Tregs) and γδ T cells. Decreased frequencies of CD4⁺ T cells and increased frequencies of Tregs and CD8⁺ γδ T cells correlated with worse outcome. Naïve CD4⁺ T cells displayed an activated phenotype with increased CD25 expression in patients with active chronic disease at 2-year follow-up. A distinctive Treg phenotype with increased expression of CD25, CTLA4, CD69, PD-1 and CD95 correlated with chronic sarcoidosis. Upon stimulation, both naïve and memory T cells displayed a different cytokine profile in sarcoidosis compared to HCs.</div></div><div><h3>Conclusions</h3><div>Circulating T cell subpopulations of sarcoidosis patients display phenotypic abnormalities that correlate with disease outcome, supporting a critical role of aberrant T cell activation in sarcoidosis pathogenesis.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103120"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49677871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of circulating and excreted metals and of autoimmunity between two Great Plains Tribal communities","authors":"Esther Erdei ,&nbsp;Elena R. O'Donald ,&nbsp;Li Luo ,&nbsp;Kendra Enright ,&nbsp;Marcia O'Leary ,&nbsp;Debra MacKenzie ,&nbsp;John Doyle ,&nbsp;Margaret Eggers ,&nbsp;Deborah Keil ,&nbsp;Johnnye Lewis ,&nbsp;Jeffrey A. Henderson ,&nbsp;Robert L. Rubin","doi":"10.1016/j.jaut.2023.103117","DOIUrl":"10.1016/j.jaut.2023.103117","url":null,"abstract":"<div><div>Metals contaminants of the environment from mine waste have been implicated as contributing agents in autoimmune disease. The current study compares metals and autoimmunity in two Tribal communities residing in the Black Hills and the Bighorn Mountains geographical regions that are scattered with extant hard rock mines. With documented drinking water contamination in both communities, <em>in vivo</em> levels of more than half of the measured serum and urine metals differed between the two communities and were substantially different from their national median values. Serum autoantibodies associated with systemic autoimmune disease were rare or at low-level, but antibodies to denatured (single-stranded) DNA and thyroid-specific autoantibodies were commonly elevated, especially in women. A three-tier statistical modeling process was carried out to examine individual metals exposure as predictors of autoantibody levels. For the most part only weak positive associations between individual metals and systemic autoantibodies were found, although univariate quantile regression analysis showed positive statistical associations of serum lead and antimony with anti-chromatin and anti-histone autoantibodies. Using age and gender-adjusted multivariable statistical models, metals did not predict anti-thyroglobulin or -thyroid peroxidase significantly and metals were generally negative predictors of the other autoantibodies. Overall these results suggest that elevated levels of environmental metals and metalloids in these communities may result in suppression of autoantibodies associated with systemic autoimmune disease.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103117"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41182635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-content multimodal analysis supports the IL-7/IL-7 receptor axis as a relevant therapeutic target in primary Sjögren's syndrome","authors":"Emiko Desvaux ,&nbsp;Patrice Hemon ,&nbsp;Perrine Soret ,&nbsp;Christelle Le Dantec ,&nbsp;Loukas Chatzis ,&nbsp;Divi Cornec ,&nbsp;Valérie Devauchelle-Pensec ,&nbsp;PRECISESADS clinical consortium ,&nbsp;Sahar Elouej ,&nbsp;Fanny Duguet ,&nbsp;Laurence Laigle ,&nbsp;Nicolas Poirier ,&nbsp;Philippe Moingeon ,&nbsp;Sylvie Bretin ,&nbsp;Jacques-Olivier Pers","doi":"10.1016/j.jaut.2023.103147","DOIUrl":"10.1016/j.jaut.2023.103147","url":null,"abstract":"<div><h3>Objective</h3><div>While the involvement of IL-7/IL-7R axis in pSS has been described in relation to T cells, little is known about the contribution of this pathway in relationship with other immune cells, and its implication in autoimmunity. Using high-content multiomics data, we aimed at characterizing IL-7R expressing cells and the involvement of IL-7/IL-7R pathway in pSS pathophysiology.</div></div><div><h3>Methods</h3><div>An <em>IL-7 signature</em> established using RNA-sequencing of human PBMCs incubated with IL-7 was applied to 304 pSS patients, and on RNA-Seq datasets from tissue biopsies. High-content immunophenotyping using flow and imaging mass cytometry was developed to characterize peripheral and <em>in situ</em> IL-7R expression.</div></div><div><h3>Results</h3><div>We identified a blood 4-gene IL-7 module (<em>IKZF4</em>, <em>KIAA0040</em>, <em>PGAP1</em> and <em>SOS1</em>) associated with anti-SSA/Ro positiveness in patients as well as disease activity, and a tissue 5-gene IL-7 module (<em>IL7R, PCED1B, TNFSF8, ADAM19, MYBL1)</em> associated with infiltration severity. We confirmed expression of IL-7R on T cells subsets, and further observed upregulation of IL-7R on double-negative (DN) B cells, and especially DN2 B cells. IL-7R expression was increased in pSS compared to sicca patients with variations seen according to the degree of infiltration. When expressed, IL-7R was mainly found on epithelial cells, CD4⁺ and CD8⁺ T cells, switched memory B cells, DN B cells and M1 macrophages.</div></div><div><h3>Conclusion</h3><div>This exhaustive characterization of the IL-7/IL-7R pathway in pSS pathophysiology established that two IL-7 gene modules discriminate pSS patients with a high IL-7 axis involvement. Their use could guide the implementation of an anti-IL-7R targeted therapy in a precision medicine approach.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103147"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138743619","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Infectious and non-infectious precipitants of sarcoidosis","authors":"Ozioma S. Chioma ,&nbsp;ZaDarreyal Wiggins ,&nbsp;Samantha Rea ,&nbsp;Wonder P. Drake","doi":"10.1016/j.jaut.2024.103239","DOIUrl":"10.1016/j.jaut.2024.103239","url":null,"abstract":"<div><div><span><span>Sarcoidosis is a chronic </span>inflammatory disease that can affect any organ in the body. Its exact cause remains unknown, but it is believed to result from a combination of genetic and </span>environmental factors<span>. Some potential causes of sarcoidosis include genetics, environmental triggers, immune system dysfunction, the gut microbiome<span><span>, sex, and race/ethnicity. Genetic mutations are associated with protection against </span>disease progression<span> or an increased susceptibility to more severe disease, while exposure to certain chemicals, bacteria, viruses, or allergens can trigger the formation of immune cell<span><span><span><span> congregations (granulomas) in different organs. Dysfunction of the immune system, including autoimmune reactions, may also contribute. The gut microbiome and factors such as being female or having African American, Scandinavian, Irish, or Puerto Rican heritage are additional contributors to disease outcome. Recent research has suggested that certain drugs, such as anti-Programmed Death-1 (PD-1) and </span>antibiotics such as tuberculosis (TB) drugs, may raise the risk of developing sarcoidosis. Hormone levels, particularly higher levels of estrogen and </span>progesterone in women, have also been linked to an increased likelihood of sarcoidosis. The diagnosis of sarcoidosis involves a comprehensive assessment that includes </span>medical history, physical examination, laboratory tests, and imaging studies. While there is no cure for sarcoidosis, the symptoms can often be effectively managed through various treatment options. Treatment may involve the use of medications, surgical interventions, or lifestyle changes. These disparate factors suggests that sarcoidosis has multiple positive and negative exacerbants on disease severity, some of which can be ameliorated and others which cannot.</span></span></span></span></div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103239"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141183717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extrapulmonary sarcoidosis","authors":"Paolo Spagnolo ,&nbsp;Vasileios Kouranos ,&nbsp;Victoria Singh-Curry ,&nbsp;Thomas El Jammal ,&nbsp;Misha Rosenbach","doi":"10.1016/j.jaut.2024.103323","DOIUrl":"10.1016/j.jaut.2024.103323","url":null,"abstract":"<div><div>Sarcoidosis is a chronic disease of unknown origin that develops when a genetically susceptible host is exposed to an antigen, leading to an exuberant immune response characterized by granulomatous inflammation. Although lung involvement is almost universal as well as the leading cause of morbidity and mortality, virtually any organ can be affected. In particular, sarcoidosis of the heart, nervous system, and eyes can be devastating, leading to death, debilitation and blindness, and a multidisciplinary approach involving expert specialists is required for prompt diagnosis and appropriate treatment. Sarcoidosis of the skin can be disfiguring, thus posing a substantial psychologic and social impact on the patients. The diagnosis is often straightforward in the presence of compatible clinical manifestations in patients with biopsy-proven sarcoidosis, but is challenging when extrapulmonary signs/symptoms occur in isolation.</div><div>Corticosteroids remain the first line therapy, with immunosuppressive or biologic agents being reserved to patients failing or experiencing side effects from steroids or developing refractory disease.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103323"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142380945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lung transplantation in pulmonary sarcoidosis","authors":"Jin Sun Kim,&nbsp;Rohit Gupta","doi":"10.1016/j.jaut.2023.103135","DOIUrl":"10.1016/j.jaut.2023.103135","url":null,"abstract":"<div><div><span><span><span>Sarcoidosis is a systemic </span>inflammatory disease of unknown etiology and variable </span>clinical course. </span>Pulmonary sarcoidosis<span><span> is the most common presentation and accounts for most morbidity and mortality related to sarcoidosis. While sarcoidosis generally has good outcomes, few patients experience chronic disease. A minority of patients progress to a specific phenotype of sarcoidosis referred to advanced pulmonary sarcoidosis (APS) which includes advanced </span>fibrosis<span><span><span>, pulmonary hypertension and respiratory failure, leading to high morbidity and mortality. In patients with advanced disease despite medical therapy, </span>lung transplantation may be the last viable option for improvement in </span>quality of life<span>. Though post-transplant survival is similar to that of other end-stage lung diseases, it is imperative that patients are evaluated and referred early to transplant centers with experience in APS. A multidisciplinary approach and clinical experience are crucial in detecting the optimal timing of referral, initiating comprehensive transplantation evaluation and listing, discussing surgical approach, and managing perioperative and post-transplant care. This review article seeks to address these aspects of lung transplantation in APS.</span></span></span></div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103135"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71481939","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A framework for exclusion of alternative diagnoses in sarcoidosis","authors":"Logan J. Harper ,&nbsp;Carol F. Farver ,&nbsp;Ruchi Yadav ,&nbsp;Daniel A. Culver","doi":"10.1016/j.jaut.2024.103288","DOIUrl":"10.1016/j.jaut.2024.103288","url":null,"abstract":"<div><div>Sarcoidosis is a multisystem granulomatous syndrome that arises from a persistent immune response to a triggering antigen(s). There is no “gold standard” test or algorithm for the diagnosis of sarcoidosis, making the diagnosis one of exclusion. The presentation of the disease varies substantially between individuals, in both the number of organs involved, and the manifestations seen in individual organs. These qualities dictate that health care providers diagnosing sarcoidosis must consider a wide range of possible alternative diagnoses, from across a range of presentations and medical specialties (infectious, inflammatory, cardiac, neurologic). Current guideline-based diagnosis of sarcoidosis recommends fulfillment of three criteria: 1) compatible clinical presentation and/or imaging 2) demonstration of granulomatous inflammation by biopsy (when possible) and, 3) exclusion of alternative causes, but do not provide guidance on standardized strategies for exclusion of alternative diagnoses. In this review, we provide a summary of the most common differential diagnoses for sarcoidosis involvement of lung, eye, skin, central nervous system, heart, liver, and kidney. We then propose a framework for testing to exclude alternative diagnoses based on pretest probability of sarcoidosis, defined as high (typical findings with sarcoidosis involvement confirmed in another organ), moderate (typical findings in a single organ), or low (atypical/findings suggesting of an alternative diagnosis). This work highlights the need for informed and careful exclusion of alternative diagnoses in sarcoidosis.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103288"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic predisposition to sarcoidosis","authors":"Shu-Yi Liao ,&nbsp;Tasha Fingerlin ,&nbsp;Lisa Maier","doi":"10.1016/j.jaut.2023.103122","DOIUrl":"10.1016/j.jaut.2023.103122","url":null,"abstract":"<div><div>Sarcoidosis is a complex systemic disease with clinical heterogeneity based on varying phenotypes and natural history. The detailed etiology of sarcoidosis remains unknown, but genetic predisposition as well as environmental exposures play a significant role in disease pathogenesis. We performed a comprehensive review of germline genetic (DNA) and transcriptomic (RNA) studies of sarcoidosis, including both previous studies and more recent findings. In this review, we provide an assessment of the following: genetic variants in sarcoidosis susceptibility and phenotypes, ancestry- and sex-specific genetic variants in sarcoidosis, shared genetic architecture between sarcoidosis and other diseases, and gene-environment interactions in sarcoidosis. We also highlight the unmet needs in sarcoidosis genetic studies, including the pressing requirement to include diverse populations and have consistent definitions of phenotypes in the sarcoidosis research community to help advance the application of genetic predisposition to sarcoidosis disease risk and manifestations.</div></div>","PeriodicalId":15245,"journal":{"name":"Journal of autoimmunity","volume":"149 ","pages":"Article 103122"},"PeriodicalIF":7.9,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49677872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}