Journal of Translational Autoimmunity最新文献

{"title":"SARS-CoV-2 and thyroid diseases","authors":"Małgorzata Staruszkiewicz ,&nbsp;Anna Pituch-Noworolska ,&nbsp;Szymon Skoczen","doi":"10.1016/j.jtauto.2023.100214","DOIUrl":"https://doi.org/10.1016/j.jtauto.2023.100214","url":null,"abstract":"<div><p>SARS-CoV-2 virus responsible for acute respiratory disease affected other organs leading to co-existence symptoms or complications. Thyroid gland was one of them due to expression of angiotensin-converting enzyme 2 (ACE2), the protein facilitating viral binding to the host cells. Moreover, thyroid gland, important for regulation of hormonal network, is extremely sensitive to any changes in homeostasis and metabolism. It was shown, that COVID-19 was associated with induction of thyroid disease or increasing existing functional disturbances or autoimmune process. Thyroid diseases are mainly based on immunological pathomechanism although the relation between immune system and thyroid function is bidirectional e.g. thyroid hormones modulate specific immune responses, including cell-mediated immunity, NK cell activity, the production of antiviral interferon (IFN) and proliferation of T- and B-lymphocytes. The effects of COVID-19 and mRNA vaccine on thyroid function and diseases are discussed.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100214"},"PeriodicalIF":3.9,"publicationDate":"2023-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49858292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Accuracy of generative artificial intelligence models in differential diagnoses of familial Mediterranean fever and deficiency of Interleukin-1 receptor antagonist","authors":"Joshua Pillai ,&nbsp;Kathryn Pillai","doi":"10.1016/j.jtauto.2023.100213","DOIUrl":"https://doi.org/10.1016/j.jtauto.2023.100213","url":null,"abstract":"<div><p>With the increasing development of artificial intelligence, large language models (LLMs) have been utilized to solve problems in natural language processing tasks. More recently, LLMs have shown unique potential in numerous applications within medicine but have been particularly investigated for their ability in clinical reasoning. Although the diagnostic accuracy of LLMs in forming differential diagnoses has been reviewed in general internal medicine applications, much is unknown in autoinflammatory disorders. From the nature of autoinflammatory diseases, forming a differential diagnosis is challenging due to the overlapping symptoms between disorders and even more difficult without genetic screening. In this work, the diagnostic accuracy of the Generative Pre-Trained Transformer Model-4 (GPT-4), GPT-3.5, and Large Language Model Meta AI (LLaMa) were evaluated in clinical vignettes of Deficiency of Interleukin-1 Receptor Antagonist (DIRA) and Familial Mediterranean Fever (FMF). We then compared these models to a control group including one internal medicine physician. It was found that GPT-4 did not significantly differ in correctly identifying DIRA and FMF patients compared to the internist. However, the physician maintained a significantly higher accuracy than GPT-3.5 and LLaMa 2 for either disease. Overall, we explore and discuss the unique potential of LLMs in diagnostics for autoimmune diseases.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100213"},"PeriodicalIF":3.9,"publicationDate":"2023-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49858293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of autoantibodies targeting interferon type 1 in COVID-19 severity: A systematic review and meta-analysis","authors":"Abolfazl Akbari ,&nbsp;Alireza Hadizadeh ,&nbsp;Mahdi Amiri ,&nbsp;Neshat Najaf Najafi ,&nbsp;Zahra Shahriari ,&nbsp;Tannaz Jamialahmadi ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.jtauto.2023.100219","DOIUrl":"10.1016/j.jtauto.2023.100219","url":null,"abstract":"<div><h3>Introduction</h3><p>Impairment of the type I interferon (IFN–I) signaling pathway is associated with increased severity of COVID-19 disease. Here we have undertaken a systematic review and meta = analysis on the association between the severity of COVID-19 and IFN-1 autoantibodies (AAbs; aIFN-1, aIFN-α, aIFN-ω, and aIFN-β).</p></div><div><h3>Methods</h3><p>Four databases, including Medline [PubMed], Embase, Web of Science, and Scopus, were systematically searched to find papers on the role of aIFN-1 and its subtype AAbs in the severity of COVID-19 infection. Data on the prevalence of aIFN-1, aIFN-α, aIFN-ω, and aIFN-β were pooled using random- or fixed-effects models. Subgroup analysis was performed based on disease severity. Odds ratios (OR) for COVID-19 disease outcome, including length of hospital stay, ICU admission and death, were calculated in relation to positive or negative plasma IFN-1 AAbs.</p></div><div><h3>Results</h3><p>A total of 33 studies with 13023 patients were included. The overall prevalence of circulating aIFN-1, aIFN-α, and aIFN-ω AAbs was 17.8 % [13.8, 22.8], 7.2 % [4.7, 10.9], and 4.4 % [2.1, 8.6], respectively, and the overall prevalence of neutralizing aIFN-1, aIFN-α, aIFN-ω, and aIFN-β AAbs was 7.1 % [4.9, 10.1], 7.5 % [5.9, 9.5], 8.0 % [5.7, 11.1] and 1.2 % [0.4, 3.5], respectively. Circulating aIFN-α (OR = 4.537 [2.247, 9.158]), neutralizing aIFN-α (O = 17.482 [8.899, 34.342]), and neutralizing aIFN-ω (OR = 12.529 [7.397, 21.222]) were significantly more frequent in critical/severe patients than in moderate/mild patients (p &lt; 0.001 for all). Anti–IFN–1 was more common in male subjects (OR = 2.248 [1.366, 3.699], p = 0.001) and two COVID-19 outcomes including ICU admission (OR = 2.485 [1.409, 4.385], p = 0.002) and death (OR = 2.593 [1.199, 5.604], p = 0.015) occurred more frequently in patients with positive anti–IFN–1.</p><p>Conclusion: aIFN-1 and its subtypes AAbs are associated with severe and critical COVID-19 disease and may be a predictive marker for a poor prognosis, particularly in men.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100219"},"PeriodicalIF":3.9,"publicationDate":"2023-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10587724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel web-based online nomogram to predict advanced liver fibrosis in patients with autoimmune hepatitis-primary biliary cholangitis overlap syndrome","authors":"Zhiyi Zhang ,&nbsp;Jian Wang ,&nbsp;Yun Chen ,&nbsp;Yiguang Li ,&nbsp;Li Zhu ,&nbsp;Huali Wang ,&nbsp;Yilin Liu ,&nbsp;Jiacheng Liu ,&nbsp;Shengxia Yin ,&nbsp;Xin Tong ,&nbsp;Xiaomin Yan ,&nbsp;Yuxin Chen ,&nbsp;Chuanwu Zhu ,&nbsp;Jie Li ,&nbsp;Yuanwang Qiu ,&nbsp;Chao Wu ,&nbsp;Rui Huang","doi":"10.1016/j.jtauto.2023.100215","DOIUrl":"https://doi.org/10.1016/j.jtauto.2023.100215","url":null,"abstract":"<div><h3>Background</h3><p>Patients with autoimmune hepatitis-primary biliary cholangitis (AIH-PBC) overlap syndrome have a worse prognosis compared to AIH or PBC alone and accurately predicting the severity and dynamically monitoring the progression of disease are therefore essential. We aimed to develop a nomogram-based model to predict advanced liver fibrosis in patients with AIH-PBC overlap syndrome.</p></div><div><h3>Methods</h3><p>A total of 121 patients with AIH-PBC overlap syndrome were retrospectively included and randomly assigned to a development set and a validation set. Backward stepwise regression's best model with the lowest AIC was employed to create a nomogram. Diagnose accuracy was evaluated using the area under the receiver operator characteristic curve (AUROC), calibration analysis, and decision curve analysis (DCA) and was compared with aspartate aminotransferase-to-platelet ratio (APRI) and fibrosis index based on four factors-4 (FIB-4) score.</p></div><div><h3>Results</h3><p>The median age of patients was 53.0 years (IQR: 46.0–63.0), and female patients accounted for 95.0 %. Platelets, globulin, total bilirubin, and prothrombin time were associated with advanced fibrosis (≥S3) and used to construct an AIH-PBC overlap syndrome fibrosis (APOSF)-nomogram (available online at <span>https://ndth-zzy.shinyapps.io/APOSF-nomogram/</span><svg><path></path></svg>). The AUROCs of APOSF-nomogram were 0.845 (95 % CI: 0.754–0.936) and 0.843 (95 % CI: 0.705–0.982) in development set and validation set respectively, which was significantly better than APRI and FIB-4. Calibration revealed that the estimated risk fits well with biopsy-proven observation. DCA outperformed APRI and FIB4 in terms of net benefit, demonstrating clinical utility.</p></div><div><h3>Conclusion</h3><p>This novel non-invasive web-based online APOSF-nomogram provided a convenient tool for identifying advanced fibrosis in patients with AIH-PBC overlap syndrome. Further prospective, multicenter studies with large sample size are necessary to validate the applicability of APOSF-nomogram.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100215"},"PeriodicalIF":3.9,"publicationDate":"2023-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49858262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"suPAR and WT1 modify the adhesion of podocytes and are related to proteinuria in class IV lupus nephritis","authors":"Juan-José Bollain-y-Goytia ,&nbsp;Felipe-de-Jesús Torres-Del-muro ,&nbsp;Sara-Paola Hernández-Martínez ,&nbsp;Esperanza Avalos-Díaz ,&nbsp;Rafael Herrera-Esparza","doi":"10.1016/j.jtauto.2023.100216","DOIUrl":"10.1016/j.jtauto.2023.100216","url":null,"abstract":"<div><h3>Introduction</h3><p>Lupus nephritis (LN) affects up to 60 % of the patients with Systemic Lupus Erythematosus (SLE) and renal damage progression is associated with proteinuria, caused in part by the integrity of the glomerular basement membrane (GBM) and by podocyte injury. The soluble urokinase plasminogen activator receptor (suPAR) and Wilms Tumor 1 (WT1) have been related to podocyte effacement and consequently with proteinuria which raises questions about its pathogenic role in LN.</p></div><div><h3>Objective</h3><p>Define whether suPAR levels and WT1 expression influence in podocyte anchorage destabilization in LN class IV.</p></div><div><h3>Materials and methods</h3><p>This is a cross-sectional study of cases and controls. We studied patients with SLE without renal involvement (n = 12), SLE and LN class IV with proteinuria ≤0.5 g/24 h (n = 12), LN class IV with proteinuria ≥0.5 g/24 h (n = 12) and compared them with renal tissue control (CR) (n = 12) and control sera (CS) (n = 12). The CR was integrated by cadaveric samples without SLE or renal involvement and the CS was integrated by healthy participants. The expression and cellular localization of WT1, urokinase-type plasminogen activator receptor (uPAR), ac-α-tubulin, vimentin, and β3-integrin was assessed by immunohistochemistry (IHC). The concentration of suPAR in serum was analyzed by enzyme-linked immunosorbent assay (ELISA).</p></div><div><h3>Results</h3><p>In patients with LN, the activation of anchoring proteins was increased, such as podocyte β3-integrin, as well as the acetylation of alpha-acetyl-tubulin and uPAR, in contrast to the decrease in vimentin; interestingly, the cellular localization of WT1 was cytoplasmic and the number of podocytes per glomerulus decreased. The concentrations of suPAR was increased in patients with LN.</p></div><div><h3>Conclusion</h3><p>The destabilization of podocyte anchorage modulated by β3-integrin activation, and tubulin acetylation, associated with decreased WT1 cytoplasmic expression, and increased suPAR levels could be involved in kidney damage in patients with LN class IV.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100216"},"PeriodicalIF":3.9,"publicationDate":"2023-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10587709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49692813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-adenylate kinase 5 encephalitis: Clinical characteristics, diagnosis, and management of this rare entity","authors":"Er-Chuang Li ,&nbsp;Qi-Lun Lai ,&nbsp;Meng-Ting Cai ,&nbsp;Gao-Li Fang ,&nbsp;Chun-Hong Shen ,&nbsp;Mei-Ping Ding ,&nbsp;Yin-Xi Zhang","doi":"10.1016/j.jtauto.2023.100218","DOIUrl":"10.1016/j.jtauto.2023.100218","url":null,"abstract":"<div><p>The spectrum and understanding of antibody-positive autoimmune encephalitis (AE) have expanded over the past few decades. In 2007, a rare subtype of AE known as anti-adenylate kinase 5 (AK5) encephalitis, was first reported. This disease is more common in elderly males, with limbic encephalitis as the core phenotype (characterized by subacute anterograde amnesia, sometimes with psychiatric symptoms, and rarely with seizures). Brain magnetic resonance imaging typically demonstrated initial temporal lobe T2/fluid-attenuated inversion recovery hyperintensities, and subsequent atrophy. No concomitant tumors have been found yet. AK5 antibody, targeting the intracellular antigen, is a biomarker for a non-paraneoplastic T-cell autoimmunity response, and can be detected in serum and cerebrospinal fluid using tissue-based and cell-based assays. Cytotoxic T-cell-mediating neuronal injury and loss play a pivotal role in the immunopathogenesis of anti-AK5 encephalitis. Patients mostly show poor response to immunotherapy and thus a poor prognosis in the long run. Herein, we review the literature and provide updated knowledge of this less-known entity, focusing on clinical characteristics, paraclinical findings, diagnosis process, and therapeutic approaches.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100218"},"PeriodicalIF":3.9,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c7/38/main.PMC10582738.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49683129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are serum C3 levels or kidney C3 deposits useful markers for predicting outcomes in patients with ANCA-associated vasculitis?","authors":"Alexis Cassard ,&nbsp;Clément Kounde ,&nbsp;Laurence Bouillet ,&nbsp;Tiphaine Goulenok ,&nbsp;David Ribes ,&nbsp;Rafik Mesbah ,&nbsp;Vincent Langlois ,&nbsp;Audrey Delas ,&nbsp;Françoise Fortenfant ,&nbsp;Sébastien Humbert ,&nbsp;Céline Lebas ,&nbsp;Julie Belliere ,&nbsp;Philippe Kerschen ,&nbsp;Dominique Chauveau ,&nbsp;Magali Colombat ,&nbsp;Stanislas Faguer","doi":"10.1016/j.jtauto.2023.100217","DOIUrl":"https://doi.org/10.1016/j.jtauto.2023.100217","url":null,"abstract":"<div><h3>Introduction</h3><p>Complement activation emerged as a key actor of anti-neutrophil cytoplasmic antibodies-associated vasculitis (AAV). Whether serum levels of C3 (sC3) or C3 kidney deposition may help to refine the prognosis of AAV remains elusive.</p></div><div><h3>Methods</h3><p>Retrospective multicentric study that included 154 patients with a first flare of AAV and sC3 (n = 143) or C3 kidney staining (n = 95) available at diagnosis. Clinical presentations, kidney pathology, and survival of patients with normal or low sC3 were compared using univariate analyses, Kaplan-Maier curves with log-rank comparison, or multivariate Cox’ model, as appropriate.</p></div><div><h3>Results</h3><p>20 patients (14 %) had low sC3. sC3 (as bivariate low/normal or as a continuous variable) was associated with 5-year mortality but not with kidney survival. C3 kidney deposition (C3+) was identified in 23 patients who were characterized by more frequent chronic hypertension and lower eGFR at presentation (p = 0.04). C3+ correlated with IgG, IgM, C1q deposition (p = 0.07, p &lt; 0.0001 and p = 0.003, respectively). Chronicity and activity scores were similar in C3+ and C3- patients. Among C3+ patients, those with C3 deposition ≥2+ had lower eGFR at presentation (p = 0.006) and were more frequently classified as sclerotic using the Berden classification (p = 0.04) and as ‘high risk’ using the Brix score (p = 0.03). However, eGFR improvement following induction regimen was similar between C3+ and C3- patients, and kidney survival at 5 years was similar.</p></div><div><h3>Conclusions</h3><p>Correlation of sC3 with mortality confirms mechanistic links between complement pathways and AAV, but the lack of clear predictive sC3 cut-off and the similar kidney outcome irrespective of C3 deposition precludes their use as biomarkers of AAV outcomes and response to treatment.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100217"},"PeriodicalIF":3.9,"publicationDate":"2023-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49858261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of COVID-19 and vaccination campaign on 1,755 systemic sclerosis patients during first three years of pandemic. Possible risks for individuals with impaired immunoreactivity to vaccine, ongoing immunomodulating treatments, and disease-related lung involvement during the next pandemic phase","authors":"Clodoveo Ferri ,&nbsp;Vincenzo Raimondo ,&nbsp;Dilia Giuggioli ,&nbsp;Laura Gragnani ,&nbsp;Serena Lorini ,&nbsp;Lorenzo Dagna ,&nbsp;Silvia Laura Bosello ,&nbsp;Rosario Foti ,&nbsp;Valeria Riccieri ,&nbsp;Serena Guiducci ,&nbsp;Giovanna Cuomo ,&nbsp;Antonio Tavoni ,&nbsp;Rossella De Angelis ,&nbsp;Fabio Cacciapaglia ,&nbsp;Elisabetta Zanatta ,&nbsp;Franco Cozzi ,&nbsp;Giuseppe Murdaca ,&nbsp;Ilaria Cavazzana ,&nbsp;Nicoletta Romeo ,&nbsp;Veronica Codullo ,&nbsp;Alessandro Antonelli","doi":"10.1016/j.jtauto.2023.100212","DOIUrl":"10.1016/j.jtauto.2023.100212","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Introduction&lt;/h3&gt;&lt;p&gt;The impact of COVID-19 pandemic represents a serious challenge for ‘frail’ patients' populations with inflammatory autoimmune systemic diseases such as systemic sclerosis (SSc). We investigated the prevalence and severity of COVID-19, as well the effects of COVID-19 vaccination campaign in a large series of SSc patients followed for the entire period (first 38 months) of pandemic.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Patients and method&lt;/h3&gt;&lt;p&gt;This prospective survey study included 1755 unselected SSc patients (186 M, 1,569F; mean age 58.7 ± 13.4SD years, mean disease duration 8.8 ± 7.3SD years) recruited in part by telephone survey at 37 referral centers from February 2020 to April 2023. The following parameters were carefully evaluated: i. demographic, clinical, serological, and therapeutical features; ii. prevalence and severity of COVID-19; and iii. safety, immunogenicity, and efficacy of COVID-19 vaccines.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;p&gt;The prevalence of COVID-19 recorded during the whole pandemic was significantly higher compared to Italian general population (47.3 % vs 43.3 %, p &lt; 0.000), as well the COVID-19-related mortality (1.91 % vs 0.72 %, p &lt; 0.001). As regards the putative prognostic factors of worse outcome, COVID-19 positive patients with SSc-related interstitial lung involvement showed significantly higher percentage of COVID-19-related hospitalization compared to those without (5.85 % vs 1.73 %; p &lt; 0.0001), as well as of mortality rate (2.01 % vs 0.4 %; p = 0.002). Over half of patients (56.3 %) received the first two plus one booster dose of vaccine; while a fourth dose was administered to 35.6 %, and only few of them (1.99 %) had five or more doses of vaccine. Of note, an impaired seroconversion was recorded in 25.6 % of individuals after the first 2 doses of vaccine, and in 8.4 % of patients also after the booster dose. Furthermore, the absence of T-cell immunoreactivity was observed in 3/7 patients tested by QuantiFERON® SARSCoV-2 Starter Set (Qiagen). The efficacy of vaccines, evaluated by comparing the COVID-19-related death rate recorded during pre- and post-vaccination pandemic periods, revealed a quite stable outcome in SSc patients &lt;em&gt;(&lt;/em&gt;death rate from 2.54 % to 1.76 %; p = ns), despite the significant drop of mortality observed in the Italian general population (from 2.95 % to 0.29 %; p &lt; 0.0001).&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;p&gt;An increased COVID-19 prevalence and mortality rate was recorded in SSc patients; moreover, the efficacy of vaccines in term of improved outcomes was less evident in SSc compared to Italian general population. This discrepancy might be explained by concomitant adverse prognostic factors: increased rate of non-responders to vaccine in SSc series, low percentage of individuals with four or more doses of vaccine, ongoing immunomodulating treatments, disease-related interstitial lung disease, and/or reduced preventive measures in the second half of pandemic. A c","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100212"},"PeriodicalIF":3.9,"publicationDate":"2023-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a5/3d/main.PMC10580042.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49683130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin-induced activation of Ca2+ signaling prevents immune infiltration/pathology in Sjogren’s syndrome-prone mouse models","authors":"Viviane Nascimento Da Conceicao ,&nbsp;Yuyang Sun ,&nbsp;Xiufang Chai ,&nbsp;Julian L. Ambrus ,&nbsp;Bibhuti B. Mishra ,&nbsp;Brij B. Singh","doi":"10.1016/j.jtauto.2023.100210","DOIUrl":"https://doi.org/10.1016/j.jtauto.2023.100210","url":null,"abstract":"<div><p>Immune cell infiltration and glandular dysfunction are the hallmarks of autoimmune diseases such as primary Sjogren’s syndrome (pSS), however, the mechanism(s) is unknown. Our data show that metformin-treatment induces <em>Ca2+ signaling that restores saliva secretion and prevents immune cell infiltration in</em> the salivary glands of IL14α-transgenic mice (IL14α), which is a model for pSS. Mechanistically, we show that loss of <em>Ca2+ signaling is a major contributing factor, which is restored by metformin treatment,</em> in IL14α mice. Furthermore, the loss of <em>Ca2+ signaling leads to ER stress in salivary glands.</em> Finally, restoration of metformin-induced <em>Ca2+ signaling</em> inhibited the release of alarmins and prevented the activation of ER stress that was essential for immune cell infiltration. These results suggest that loss of metformin-mediated activation of <em>Ca2+</em> signaling prevents ER stress, which inhibited the release of alarmins that induces immune cell infiltration leading to salivary gland dysfunction observed in pSS.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100210"},"PeriodicalIF":3.9,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49858294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paradoxical psoriasis: The flip side of idiopathic psoriasis or an autocephalous reversible drug reaction?","authors":"Jiawei Lu,&nbsp;Yan Lu","doi":"10.1016/j.jtauto.2023.100211","DOIUrl":"10.1016/j.jtauto.2023.100211","url":null,"abstract":"<div><p>Psoriasis is a common, chronic skin disease that results mainly from the complex interplay between T cells, dendritic cells, and inflammatory cytokines including TNF-α, IL-17, IL-12, and IL-23. Successful therapy with anti-cytokine antibodies has proved the importance of these key cytokines, especially TNF-α. During the <em>anti</em>-TNF-α treatment of classical idiopathic psoriasis, a small portion of patients develop new psoriasiform lesions. This contradictory phenomenon was named paradoxical psoriasis which resembles idiopathic psoriasis clinically but presents overlapped histological patterns and distinct immunological processes. In this review, we discuss the differences between idiopathic psoriasis and paradoxical psoriasis with an emphasis on their innate immunity, as it is predominant in paradoxical psoriasis which exhibits type I IFN-mediated immunity without the activation of autoreactive T cells and memory T cells. We also put up an instructive algorithm for the management of paradoxical psoriasis. The decision on drug discontinuation or switching of biologics should be made based on the condition of underlying diseases and the severity of lesions.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"7 ","pages":"Article 100211"},"PeriodicalIF":3.9,"publicationDate":"2023-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b0/49/main.PMC10507642.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41151299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}