Autoimmunity reviews最新文献

{"title":"Association between Omega-3 fatty acids and autoimmune disease: Evidence from the umbrella review and Mendelian randomization analysis","authors":"Kimsor Hong ,&nbsp;Marady Hun ,&nbsp;Feifeng Wu ,&nbsp;Jueyi Mao ,&nbsp;Yang Wang ,&nbsp;Junquan Zhu ,&nbsp;Xin Zhou ,&nbsp;Haotian Xie ,&nbsp;Jidong Tian ,&nbsp;Chuan Wen","doi":"10.1016/j.autrev.2024.103651","DOIUrl":"10.1016/j.autrev.2024.103651","url":null,"abstract":"<div><h3>Background</h3><div>Autoimmune diseases are a group of disorders characterized by abnormal immune responses that mistakenly target and attack healthy cells, tissues, and organs, resulting in inflammation and tissue damage. Omega-3 fatty acids possess anti-inflammatory activities and may decrease abnormal immune activity. However, the role of omega-3 fatty acids in various autoimmune diseases is still unclear. This umbrella review and Mendelian randomization (MR) study aims to summarize the highest available evidence on omega-3 fatty acids and autoimmune disease.</div></div><div><h3>Methods</h3><div>We conducted an umbrella review by searching electronic databases to identify systematic reviews and meta-analyses. The selection criteria included systematic reviews with or without meta-analysis, which evaluated omega-3 fatty acids as the exposure and autoimmune disease as the outcome variable. Two authors independently assessed the overlapping and quality of the reviews using the AMSTAR-2 tool. We also performed MR studies to investigate the potential causal effect of fatty acids on the risk of various autoimmune diseases, utilizing data from the meta-analysis of the UKB-TOPMed and FinnGen cohorts.</div></div><div><h3>Result</h3><div>The umbrella review identified 21 studies (8 systematic reviews and 13 meta-analyses) on 9 autoimmune diseases and 30 diseases in the MR study. AMSTAR 2 categorized the quality of evidence in six studies as critically low, six studies as low, eight studies as moderate, and one as high-quality evidence. The consistent result between the review and the MR study demonstrated the benefit of omega-3 fatty acids on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Additionally, in our summary review, omega-3 fatty acids can improve disease activity and inflammation biomarkers; however, MR studies provided no consistent evidence for the causal effects of omega-3 fatty acids on psoriasis, multiple sclerosis (MS), type 1 diabetes (T1D), IgA nephropathy (IgAN), juvenile idiopathic arthritis (JIA), Crohn's disease (CD), and ulcerative colitis (UC).</div></div><div><h3>Conclusion</h3><div>The current study presented solid evidence highlighting the advantageous impact of omega-3 fatty acids on SLE and RA. This was achieved through the reduction of disease risk, the decrease of disease activity, and the mitigation of inflammatory biomarkers. To stratify another autoimmune illness, it is necessary to carry out rigorous evaluations to surpass the existing findings and enhance understanding in this domain.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103651"},"PeriodicalIF":9.2,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364191","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":"Tyrosine kinase 2 inhibitors in autoimmune diseases","authors":"Chethana Ramakrishna ,&nbsp;Alice Mason ,&nbsp;Christopher J. Edwards","doi":"10.1016/j.autrev.2024.103649","DOIUrl":"10.1016/j.autrev.2024.103649","url":null,"abstract":"<div><div>Tyk2 is a member of the JAK kinase family. It is an important mediator in pro-inflammatory signalling, implicated in both innate and adaptive immune system. Activation of Tyk2 is believed to be integral to cellular processes that contribute to the development and progression of autoimmune disorders. Selective targeting of Tyk2 may reduce the number of adverse events as compared to non-selective JAK inhibitors. Therefore, in recent years there has been a growing body of research examining the inhibition of Tyk2 as a therapeutic intervention in autoimmune disease. Deucravacitinib has been approved for the treatment of moderate to severe skin psoriasis. This drug and other novel Tyk2 inhibitors are now being explored as therapies for multiple autoimmune diseases, including psoriatic arthritis, SLE, Sjogren's, dermatomyositis, inflammatory bowel disease, uveitis, hidradenitis suppurativa and others. Tyk2 inhibitors offer a potentially exciting new treatment option across a wide range of autoimmune diseases. We discuss Tyk2 inhibition, the current evidence for its usage to date, ongoing trials and what the future might hold.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103649"},"PeriodicalIF":9.2,"publicationDate":"2024-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340219","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":"Cutting edge confusion about cut-off settings in autoimmune diagnostics","authors":"Jan Damoiseaux ,&nbsp;Hetty Bontkes ,&nbsp;Leontine Mulder","doi":"10.1016/j.autrev.2024.103650","DOIUrl":"10.1016/j.autrev.2024.103650","url":null,"abstract":"<div><div>In autoimmune diagnostics results are interpreted in relation to a single or multiple cut-off value(s) in order to decide if the test is negative, weak positive, positive, or even strong positive. The way a cut-off is established appears to be very heterogeneous and this hampers harmonization of test results obtained in assays, either established in-house or obtained from different companies. In this context it is surprising that in diagnostic and classification criteria for distinct autoimmune diseases referral is made to cut-off values with the intention of harmonization. In this review article distinct ways to establish cut-off values will be described and discussed in relation to some disease criteria in order to increase the awareness of the confusion matrix of cut-off values and, as a consequence, the implications for test result interpretation.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103650"},"PeriodicalIF":9.2,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340216","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":"Indian Rheumatology Association guidelines for the management of ANCA associated vasculitis","authors":"Aadhaar Dhooria ,&nbsp;G.S.R.S.N.K. Naidu ,&nbsp;Durga Prasanna Misra ,&nbsp;Benzeeta Pinto ,&nbsp;M.B. Adarsh ,&nbsp;Saket Jha ,&nbsp;Rajiv Ranjan Kumar ,&nbsp;Arghya Chattopadhyay ,&nbsp;Vikas Sharma ,&nbsp;Debashish Mishra ,&nbsp;Nupoor Acharya ,&nbsp;Sakshi Mittal ,&nbsp;Siddharth Jain ,&nbsp;Joydeep Samanta ,&nbsp;Chengappa Kavadichanda ,&nbsp;Sahajal Dhooria ,&nbsp;Raja Ramachandran ,&nbsp;Ramesh Jois ,&nbsp;Banwari Sharma ,&nbsp;Canchi Balakrishnan ,&nbsp;Aman Sharma","doi":"10.1016/j.autrev.2024.103647","DOIUrl":"10.1016/j.autrev.2024.103647","url":null,"abstract":"<div><h3>Background</h3><div>The ACR in 2021 and the EULAR in 2022 published recommendations for management of ANCA-associated vasculitis. Given the differences in the demographic, clinical profiles, and the socio-economic realities between various countries, there is a need for development of guidelines for the management of AAV for less economically developed regions of the world.</div></div><div><h3>Methods</h3><div>These guidelines were made following the GRADE methodology. After the systematic literature review, recommendations were formulated and opinion was sought from the 18-member expert panel consisting of 17 clinicians and one patient representative.</div></div><div><h3>Results</h3><div>Twenty recommendations were formulated. We recommend ANCA testing by ELISA over IIF. For remission induction in active GPA or MPA, we recommend use of intravenous cyclophosphamide or rituximab in combination with glucocorticoids. We conditionally recommend the use of reduced dose glucocorticoids over standard dose glucocorticoids for remission induction in active GPA or MPA. For remission maintenance in patients with GPA or MPA, we recommend the use of rituximab over azathioprine for at least 48 months from diagnosis. We conditionally recommend the use of plasma exchange in patients with severe renal vasculitis. For remission induction in EGPA, we recommend use of cyclophosphamide or rituximab in severe disease and mepolizumab or azathioprine or methotrexate or mycophenolate mofetil in non-severe disease.</div></div><div><h3>Conclusions</h3><div>These are the first ever Indian recommendations for the management of AAV. Despite our effort to formulate these recommendations based on high quality evidence, some recommendations were still based on low quality evidence but with high rate of agreement among expert panel members.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103647"},"PeriodicalIF":9.2,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142340218","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":"Cardiovascular disease risk in systemic lupus erythematous: Certainties and controversies","authors":"Fabiola Atzeni ,&nbsp;Ignasi Rodríguez-Pintó ,&nbsp;Ricard Cervera","doi":"10.1016/j.autrev.2024.103646","DOIUrl":"10.1016/j.autrev.2024.103646","url":null,"abstract":"<div><div>Patients with systemic lupus erythematosus (SLE) experience greater cardiovascular morbidity and mortality compared to the general population. It is known that endothelial dysfunction, an early indicator of atherosclerosis development, can arise even without the presence of conventional cardiovascular risk factors. In fact, the risk factors contributing to cardiovascular disease can be classified into traditional risk factors and those uniquely associated with SLE such as disease activity, autoantibodies, etc.Furthermore, the pathogenesis of cardiovascular disease in SLE is linked to the activation of both the innate and adaptive immune systems. Given these findings, it is essential for clinicians to acknowledge the heightened CVD risk in SLE patients, perform comprehensive screenings for cardiovascular risk factors, and implement aggressive treatment strategies for those who exhibit signs of clinical CVD. The aim of this review is to summarize the findings on cardiovascular disease in SLE and to examine potential screening and therapeutic strategies for clinical practice.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 10","pages":"Article 103646"},"PeriodicalIF":9.2,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328035","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":"An immunology model for accelerated coronary atherosclerosis and unexplained sudden death in the COVID-19 era","authors":"Dennis McGonagle ,&nbsp;Sami Giryes","doi":"10.1016/j.autrev.2024.103642","DOIUrl":"10.1016/j.autrev.2024.103642","url":null,"abstract":"<div><div>The immunological basis for cardiac deaths remote from potential triggering viral infection, including SARS-CoV-2 infection, remains enigmatic. Cardiac surface inflammation, including the pericardium, epicardium and superficial myocardium with associated coronary artery vasculitis in infant Kawasaki Disease (KD) and multisystem inflammatory syndrome in children (MIS-C) is well recognised. In this perspective, we review the evidence pointing towards prominent post-viral infection related epicardial inflammation in older subjects, resulting in atherosclerotic plaque destabilisation with seemingly unrelated myocardial infarction that may be temporally distant from the actual infectious triggers. Cardiac surface inflammation in the relatively immune cell rich tissues in the territory though where the coronary arteries traverse is common in the adult post-COVD pneumonic phase and is also well described after vaccination including pre-COVID era vaccinations. Immunologically, the pericardium/epicardium tissue was known to be critical for coronary artery territory atherosclerotic disease prior to the COVID-19 era and may be linked to the involvement of the coronary artery vasa vasorum that physiologically oxygenates the coronary artery walls. We highlight how viral infection or vaccination-associated diffuse epicardial tissue inflammation adjacent to the coronary artery vasa vasorum territory represents a critical unifying concept for seemingly unrelated fatal coronary artery atherosclerotic disease, that could occur soon after or remote from infection or vaccination in adults. Mechanistically, such epicardial inflammation impacting coronary artery vasa vasorum immunity acts as gateways towards the slow destabilisation of pre-existing atherosclerotic plaques, with resultant myocardial infarction and other cardiac pathology. This model offers immunologists and academic cardiologists an immunopathological roadmap between innocuous viral infections or vaccinations and seemingly temporally remote “unrelated” atherosclerotic disease with excess cardiac deaths.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103642"},"PeriodicalIF":9.2,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307014","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":"Assessing recruitment and retention strategies in clinical trials for inequitable populations in systemic lupus erythematosus: A cross-sectional analysis","authors":"Kaylyn Rowsey ,&nbsp;Seth Sims ,&nbsp;Merhawit Ghebrehiwet ,&nbsp;Andrew Wilson ,&nbsp;Josh Autaubo ,&nbsp;Payton Clark ,&nbsp;Simran Demla ,&nbsp;Alicia Ito Ford ,&nbsp;Matt Vassar","doi":"10.1016/j.autrev.2024.103645","DOIUrl":"10.1016/j.autrev.2024.103645","url":null,"abstract":"<div><h3>Background</h3><p>Systemic lupus erythematosus (SLE) exhibits a mortality rate four times higher in historically marginalized populations compared to the general population. It is essential for clinical trials to accurately represent the disease population to effectively evaluate treatment modalities. However, the current trial design lacks appropriate diversity, limiting the generalizability of results. We aim to assess the recruitment and retention strategies of historically marginalized populations in SLE clinical trials.</p></div><div><h3>Methods</h3><p>In this cross-sectional analysis, relevant clinical trials were obtained in a comprehensive search of MEDLINE (PubMed) and Embase (Elsevier) in May of 2024. Included trials were published between January 1, 2018, and December 31, 2023, with a focus on SLE interventions. Reviewers KR and SS independently performed screening and data extraction via a standardized Google Form. The main outcome measured was the usage of recruitment and retention strategies, concerning under-resourced populations. All statistical analyses were performed via Stata 18 SE.</p></div><div><h3>Findings</h3><p>Our initial database search returned 747 trials, but only 86 were included in this sample. Of these, 4/86 (4.7 %) implemented recruitment strategies while 6/86 (7.0 %) reported the use of specific retention strategies. Nineteen of the 86 studies (22.1 %) reported challenges to the recruitment of inequitable populations, primarily identifying the disproportionate representation of female participants and socioeconomic obstacles as a limitation.</p></div><div><h3>Interpretation</h3><p>Key strengths include a thorough methodology from adherence to PRISMA guidelines and generalizable findings with the inclusion of international trials. Limitations include publication bias and exclusion of trials in non-English languages. Our study highlights the need for practical initiation of effective recruitment and retention strategies that aim to engage historically marginalized populations in SLE clinical trials. Addressing these gaps is necessary to prioritize the participation of inequitable populations, increase standardization of SLE treatments, and improve the relevance of SLE research.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103645"},"PeriodicalIF":9.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142274689","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":"Prolactin's paradox: Friend, foe, or both in immune regulation?","authors":"Vânia Borba ,&nbsp;Pedro Carrera-Bastos ,&nbsp;Gisele Zandman-Goddard ,&nbsp;Alejandro Lucia ,&nbsp;Yehuda Shoenfeld","doi":"10.1016/j.autrev.2024.103643","DOIUrl":"10.1016/j.autrev.2024.103643","url":null,"abstract":"<div><div>Over 100 diseases have been recognized as autoimmune in nature, collectively affecting ∼20 % of the population in industrialized countries. These conditions are more prevalent among women of childbearing age, reflecting the potential association between alterations in the immune-neuroendocrine network, on the one hand, and autoimmune conditions, on the other. Prolactin (PRL), a polypeptide hormone that is primarily (but not only) secreted by the lactotrophic cells of the pituitary gland, is a critical element of the immune-neuroendocrine network. Although this hormone has several nonimmune functions, its role in regulating immune responses and affecting autoimmune inflammation is particularly enigmatic and controversial. Indeed, PRL interacts with various immune cells to bolster the body defenses, but also potentially to exacerbate autoimmune conditions. Understanding how and when PRL acts as a ‘friend or foe’ is crucial for unraveling its role as a potential therapeutic target in the management of autoimmune diseases (AIDs). This review therefore provides a critical overview of PRL's role in the immune system, and of the influence of this pleiotropic hormone in the development of autoimmunity.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103643"},"PeriodicalIF":9.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279914","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":"Inclusion body myositis: Correcting impaired mitochondrial and lysosomal autophagy as a potential therapeutic strategy","authors":"Stefen Brady ,&nbsp;Joanna Poulton ,&nbsp;Sylviane Muller","doi":"10.1016/j.autrev.2024.103644","DOIUrl":"10.1016/j.autrev.2024.103644","url":null,"abstract":"<div><div>Inclusion body myositis (IBM) is a late onset sporadic myopathy with a characteristic clinical presentation, but as yet unknown aetiology or effective treatment. Typical clinical features are early predominant asymmetric weakness of finger flexor and knee extensor muscles. Muscle biopsy shows endomysial inflammatory infiltrate, mitochondrial changes, and protein aggregation. Proteostasis (protein turnover) appears to be impaired, linked to potentially dysregulated chaperone-mediated autophagy and mitophagy (a type of mitochondrial quality control). In this review, we bring together the most recent clinical and biological data describing IBM. We then address the question of diagnosing this pathology and the relevance of the current biological markers that characterize IBM. In these descriptions, we put a particular emphasis on data related to the deregulation of autophagic processes and to the mitochondrial-lysosomal crosstalk. Finally, after a short description of current treatments, an overview is provided pointing towards novel therapeutic targets and emerging regulatory molecules that are being explored for treating IBM. Special attention is paid to autophagy inhibitors that may offer innovative breakthrough therapies for patients with IBM.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103644"},"PeriodicalIF":9.2,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142279912","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":"Targeting ferroptosis in autoimmune diseases: Mechanisms and therapeutic prospects","authors":"Yingzi Zheng ,&nbsp;Fangfang Yan ,&nbsp;Shasha He ,&nbsp;Lianxiang Luo","doi":"10.1016/j.autrev.2024.103640","DOIUrl":"10.1016/j.autrev.2024.103640","url":null,"abstract":"<div><p>Ferroptosis is a form of regulated cell death that relies on iron and exhibits unique characteristics, including disrupted iron balance, reduced antioxidant defenses, and abnormal lipid peroxidation. Recent research suggests that ferroptosis is associated with the onset and progression of autoimmune disorders such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and multiple sclerosis (MS). However, the precise effects and molecular mechanisms remain incompletely understood. This article presents an overview of how ferroptosis mechanisms contribute to the development and advancement of autoimmune diseases, as well as the involvement of various immune cells in linking ferroptosis to autoimmune conditions. It also explores potential drug targets within the ferroptosis pathway and recent advancements in therapeutic approaches aimed at preventing and treating autoimmune diseases by targeting ferroptosis. Lastly, the article discusses the challenges and opportunities in utilizing ferroptosis as a potential therapeutic avenue for autoimmune disorders.</p></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"23 11","pages":"Article 103640"},"PeriodicalIF":9.2,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142274688","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}