Journal of Translational Autoimmunity最新文献

{"title":"Understanding the role of immune-mediated inflammatory disease related cytokines interleukin 17 and 23 in pregnancy: A systematic review","authors":"Aniek Plug ,&nbsp;Liana Barenbrug ,&nbsp;Bart G.J. Moerings ,&nbsp;Elke M.G. de Jong ,&nbsp;Renate G. van der Molen","doi":"10.1016/j.jtauto.2025.100279","DOIUrl":"10.1016/j.jtauto.2025.100279","url":null,"abstract":"<div><h3>Background</h3><div>Pregnancy requires a careful immune balance between tolerance for the semi-allogenic fetus and protection against pathogens. Women with immune-mediated inflammatory diseases (IMIDs), where the interleukin (IL)-23/IL-17 axis plays an important role, often experience changes in disease severity during pregnancy. These changes and the association between disease flares and pregnancy complications, suggests a role for IL-17 and IL-23 in pregnancy.</div></div><div><h3>Methods</h3><div>We systemically searched PubMed, EMBASE, and Web of Science (March 2024), to assess the role of IL-17 and IL-23 in pregnancy-related <em>in vitro</em> assays, animal or human studies.</div></div><div><h3>Results</h3><div>Eighty articles (8 <em>in vitro</em>, 11 animal and 61 human studies) were included. Seventy-one studies reported on IL-17 and 16 studies on IL-23. <em>In vitro</em> trophoblast proliferation, migration and invasion was increased in the presence of IL-17, but impaired with IL-23. IL-17 levels were increased in animal models for pregnancy complications. In humans, IL-17 levels seemed to be increased in pregnant women versus non-pregnant women. Additionally, elevated IL-17 levels were associated with pregnancy complications. Although similar trends were found for IL-23, data were limited.</div></div><div><h3>Conclusions</h3><div>We identified a large, but heterogenic, body of evidence for a significant role of IL-17 in all stages of pregnancy: while an excessive increase seemed to be associated with complications. The limited number of studies prevents firm conclusions on the role of IL-23. Future research is needed to find biomarkers for patients with IMIDs to predict the effect of possible disease flares on pregnancy, and the effect of therapeutic inhibition of IL-17 or IL-23.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100279"},"PeriodicalIF":4.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143403512","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":"Enhancement of CD8+T cell cytotoxicity activity by IFN-α implies alternative pathologic role in systemic lupus erythematosus","authors":"Chen-xing Zhang ,&nbsp;You-ying Mao ,&nbsp;Yu-pin Tan ,&nbsp;Mei-yu Zhang ,&nbsp;Kang Shao ,&nbsp;Shu-jun Wang ,&nbsp;Ping Ji ,&nbsp;Jia-yuan Wang ,&nbsp;Lei Yin ,&nbsp;Ying Wang","doi":"10.1016/j.jtauto.2025.100276","DOIUrl":"10.1016/j.jtauto.2025.100276","url":null,"abstract":"<div><h3>Objective</h3><div>Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease which is affected by the environmental, genetic factors as well as the immune system. Previous reports have implicated IFN-α in the pathogenesis of SLE. Up to date, however, no research has ever investigated the effect of IFN-α on CD8⁺T cells, which might be implicated in the pathogenesis of SLE. In the present study, we aimed to explore the pathologic role of IFN-α in regard to dysfunction of CD8⁺T cells in SLE.</div></div><div><h3>Methods</h3><div>Serum level of IFN-α was detected in SLE and healthy controls (HC). Surface expression of lysosome-associated membrane protein 1 (LAMP-1; CD107a) and secretion of granzyme B of CD8⁺T cells was measured in SLE and HC with or without IFN-α co-stimulation/PI3K inhibitor.</div></div><div><h3>Results</h3><div>Our results demonstrated that there was increased surface expression of CD107a of CD8⁺T cells in SLE patients compared with healthy controls (HC), indicating enhanced cytotoxicity of CD8⁺T cells in SLE patients. Meanwhile, increased secretion of granzyme B was also detected in CD8⁺T cells of SLE compared with HC, which correlated with the disease activity (SLEDAI). Furthermore, elevated serum level of IFN-α in SLE was confirmed in our study. In vitro study, granzyme B secretion by CD8⁺T cells was upregulated upon IFN-α costimulation, which was consistent with enhanced cytotoxicity of CD8⁺T cells upon IFN-α costimulation, as reflected by elevated surface expression of CD107a. PI3K inhibitor reversed increased granzyme B synthesis upon IFN-α costimulation in a dose-dependent manner.</div></div><div><h3>Conclusion</h3><div>In summary, elevated serum level of IFN-α was responsible for increased secretion of granzyme B and enhanced cytotoxicity of CD8⁺T cells in SLE and this process may be related to PI3K pathway. Relevant molecules and mechanism remains to be explored in the future.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100276"},"PeriodicalIF":4.7,"publicationDate":"2025-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143372068","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":"The follow-up of patients with celiac disease","authors":"Marco Di Tola ,&nbsp;Hetty J. Bontkes ,&nbsp;Juan Irure-Ventura ,&nbsp;Marcos López-Hoyos ,&nbsp;Nicola Bizzaro","doi":"10.1016/j.jtauto.2025.100278","DOIUrl":"10.1016/j.jtauto.2025.100278","url":null,"abstract":"<div><div>Celiac disease (CD) is a very common immune-mediated enteropathy resulting from the interaction between dietary gluten and the immune system in genetically predisposed individuals. The immune response leads to intestinal damage, malabsorption and, ultimately, to a broad spectrum of both intestinal and extra-intestinal symptoms. According to current criteria, a proper diagnosis of CD requires an initial phase consisting of clinical case identification and serological screening that, over time, has increased in importance. In most adults and in selected children, the diagnosis is subsequently defined by histological evidence of intestinal damage as a confirmatory test, which usually returns to normal after a suitable period of a gluten-free diet (GFD). The clinical remission and disappearance of circulating antibodies after a GFD further confirm the diagnosis and represent a goal to be achieved to improve the quality of life and reduce the risk of long-term complications. However, although the diagnostic criteria for CD are well defined and described in specific guidelines, the monitoring of CD patients undergoing GFD has been less studied and, consequently, specific guidelines for this phase are still lacking. The aim of this report was to evaluate the classical tools used to monitor the adherence and response to GFD, other non-invasive biomarkers that have been proposed for CD monitoring, and the histological follow-up of CD patients in order to provide a starting point for future discussions on this specific topic.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100278"},"PeriodicalIF":4.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143174021","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":"The antibody repertoire of autoimmune sensory neuronopathies targets pathways of the innate and adaptive immune system. An autoantigenomic approach","authors":"Christian P. Moritz ,&nbsp;Yannick Tholance ,&nbsp;Nadia Boutahar ,&nbsp;Coralie Borowczyk ,&nbsp;Anne-Emmanuelle Berger ,&nbsp;Stéphane Paul ,&nbsp;Jean-Christophe Antoine ,&nbsp;Jean-Philippe Camdessanché","doi":"10.1016/j.jtauto.2025.100277","DOIUrl":"10.1016/j.jtauto.2025.100277","url":null,"abstract":"<div><div>Sensory neuronopathies (SNN) encompass diverse etiologies, with autoimmunity playing a major role through both cellular and humoral responses. To investigate the humoral autoantibody repertoire in autoimmune SNN, we conducted a retrospective cohort study using large Human Proteome-wide protein microarrays (HuProt 3.1, HuProt 4.0, ProtoArrays). We specifically analyzed immune system pathways targeted within the autoantigen repertoire (the autoantigenome). We included 131 participants: 44 patients with non-paraneoplastic autoimmune SNN (12 with anti-FGFR3 and/or anti-AGO antibodies), 8 with paraneoplastic SNN, and 79 controls. Findings were validated in an independent cohort of 16 SNN patients. Overrepresentation of immune-system-related proteins was assessed using the Reactome database, and serum levels of IFN-γ and IL-6 were measured with the Bio-Plex Pro™ Reagent Kit. Autoimmune SNN sera interact with significantly more immune system proteins than healthy controls (ProtoArrays: 271/863 vs. 14/863, HuProt: 112/1694 vs. 39/1694, both p &lt; 0.0001). Overrepresentation was observed across all major immune sub-pathways, including innate and adaptive immune responses as well as cytokine signaling. Anti-FGFR3-positive SNN patients showed more frequent reactivity to immune system proteins than anti-FGFR3-negative ones. The independent SNN cohort validated the overrepresentation of targeted immune system pathways. Validation with dot blot and ELISA confirmed reactivity to TRIM21 and IL-6 and identified anti-IFN-γ-positive SNN patients. IFN-γ levels correlated weakly with levels of anti-IFN-γ antibodies (Pearson's <em>r</em> = 0.22, p = 0.03). We conclude that the antibody repertoire of autoimmune SNN targets pathways of the innate and adaptive immune system, potentially reflecting key disease-related immune pathways and highlighting the systemic role of immune dysregulation in SNN.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100277"},"PeriodicalIF":4.7,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143387270","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":"Helicobacter mastomyrinus infection induces autoimmune hepatitis in mice","authors":"Liqi Zhu ,&nbsp;Yuanyuan Liang ,&nbsp;Linghan Yang ,&nbsp;Qihui Yang ,&nbsp;Jun Yin ,&nbsp;Tao Wang ,&nbsp;Xiangming Xu ,&nbsp;Quan Zhang","doi":"10.1016/j.jtauto.2025.100275","DOIUrl":"10.1016/j.jtauto.2025.100275","url":null,"abstract":"<div><h3>Background</h3><div>Autoimmune hepatitis (AIH) is a chronic progressive liver disease caused by the immune system mistakenly attacking its own hepatocytes. The role of the gut microbiome in the pathogenesis and progression of AIH is of considerable significance. However, the dearth of suitable animal models has significantly constrained advancements in the pathogenesis and the development of therapeutic strategies for AIH. <em>Helicobacter mastomyrinus</em> (<em>H. mastomyrinus,</em> Hm) is a potentially zoonotic pathogenic microorganism capable of causing diseases of the enterohepatic system in rodent laboratory animals. Nevertheless, research on its role and mechanisms in causing liver disease is severely limited.</div></div><div><h3>Methods</h3><div>In this study, male BALB/c mice were infected with Hm isolate Hm-17, and were sacrificed at 4 w, 8 w, 14 w and 22 w after infection, respectively. The serum was collected for detecting a number of AIH indicators, including the aminotransferases level, IgG content and autoantibody level. Additionally, the liver tissue was examined for pathological analysis, fibrosis, bacterial content, and the distribution of immune cells.</div></div><div><h3>Results</h3><div>It was observed that the infection initially caused focal necrotizing hepatitis and subsequently progressed to interface hepatitis with lymphocyte/plasma cell infiltration, as well as hypergammaglobulinemia and autoantibody reactions, predominantly to Anti-nuclear and anti-smooth muscle antibodies. Furthermore, as the infection persisted, the mice exhibited a progressive increase in liver fibrosis and mild steatosis. Despite the maintenance of a low level of Hm colonization in the liver, there was a notable infiltrate of macrophages, T and B lymphocytes. In particular, the inflammatory foci in the Hm-infected liver were highly enriched for IL17⁺ cells.</div></div><div><h3>Conclusion</h3><div>The present study provides an animal model of immunological liver injury induced by Hm infection that exhibits main characteristics similar to those observed in AIH-1 patients. This model may serve as a novel animal model for the study of the pathogenesis and potential therapeutic strategies for human AIH.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100275"},"PeriodicalIF":4.7,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143174953","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":"Aberrant B cell receptor signaling responses in circulating double-negative 2 B cells from radiographic axial spondyloarthritis patients","authors":"Rick Wilbrink ,&nbsp;Stefan F.H. Neys ,&nbsp;Rudi W. Hendriks ,&nbsp;Anneke Spoorenberg ,&nbsp;Frans G.M. Kroese ,&nbsp;Odilia B.J. Corneth ,&nbsp;Gwenny M.P.J. Verstappen","doi":"10.1016/j.jtauto.2025.100270","DOIUrl":"10.1016/j.jtauto.2025.100270","url":null,"abstract":"<div><h3>Objective</h3><div>Radiographic axial spondyloarthritis (r-axSpA) is a chronic rheumatic disease in which innate immune cells and T cells are thought to play a major role. However, recent studies also hint at B cell involvement. Here, we performed an in-depth analysis on alterations within the B-cell compartment from r-axSpA patients.</div></div><div><h3>Methods</h3><div>We performed immune gene expression profiling on total peripheral blood B cells from 8 r-axSpA patients and 8 healthy controls (HCs). Next, we explored B cell subset distribution and B-cell receptor (BCR) signaling responses in circulating B cells from 28 r-axSpA patients and 15 HCs, by measuring spleen tyrosine kinase, phosphoinositide 3-kinase and extracellular signal regulated kinase 1/2 phosphorylation upon α-Ig stimulation using phosphoflow cytometry.</div></div><div><h3>Results</h3><div>Immune gene expression profiling indicated an elevated pathway score for BCR signaling in total B cells from r-axSpA patients compared with HCs. Flow cytometric analysis revealed an increase in frequency of both total and double-negative 2 (DN2) B cells in r-axSpA patients compared with HCs. In r-axSpA patients, DN2 B cells displayed an isotype shift towards IgA. Remarkably, where DN2 B cells from HCs were hyporesponsive, these cells displayed significant proximal BCR signaling responses in r-axSpA patients. Enhanced BCR signaling responses were also observed in the transitional and naïve B cell population from r-axSpA patients compared with HCs. The enhanced BCR signaling responses in DN2 B cells correlated with clinical disease parameters.</div></div><div><h3>Conclusion</h3><div>In r-axSpA patients, circulating DN2 B cells are expanded and, together with transitional and naïve B cells, display significantly enhanced BCR signaling responses upon stimulation. Together, our data suggest B cell involvement in the pathogenesis of r-axSpA.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100270"},"PeriodicalIF":4.7,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143175347","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":"Tofacitinib downregulates JAK1 and JAK3 on human intestinal monocytes and macrophages without affecting dendritic cells phenotype or function","authors":"Elisa Arribas-Rodríguez ,&nbsp;Ángel De Prado ,&nbsp;Beatriz de Andrés ,&nbsp;Benito Velayos ,&nbsp;Jesús Barrio ,&nbsp;Alejandro Romero ,&nbsp;Francisco Javier García-Alonso ,&nbsp;Álvaro Martín-Muñoz ,&nbsp;José A. Garrote ,&nbsp;Eduardo Arranz ,&nbsp;Luis Fernández-Salazar ,&nbsp;David Bernardo","doi":"10.1016/j.jtauto.2025.100271","DOIUrl":"10.1016/j.jtauto.2025.100271","url":null,"abstract":"<div><h3>Background</h3><div>Ulcerative colitis (UC) is an inflammatory disorder of the gastrointestinal tract. Although Tofacitinib, which inhibits the JAK1 and JAK3 signalling pathway, is approved to treat patients with UC, its specific mechanism of action remain elusive. Given the central role that conventional dendritic cells (cDC) elicit in gut homeostasis, we hypothesised that Tofacitinib acts modulating cDC function in UC.</div></div><div><h3>Methods</h3><div>Human biopsies were obtained from colon of controls, and patients with UC (active and quiescent). Lamina propria mononuclear cells (LPMC) were <em>ex-vivo</em> cultured in the presence/absence of Tofacitinib. The specific effect elicited over human intestinal cDC, monocytes and macrophages was assessed by flow cytometry. cDC were also enriched following Tofacitinib conditioning in order to assess its effect over naïve T-cells.</div></div><div><h3>Results</h3><div>Several human intestinal cDC, monocyte and macrophage subsets can be found in the human colon, with these cells being more similar between controls and patients with qUC referred to patients with aUC. Following <em>ex-vivo</em> culture, Tofacitinib downregulated JAK1 expression on intestinal monocytes from patients with both active and quiescent UC. As for macrophages, JAK1 was decreased on patients with active UC while JAK was downregulated on macrophages from patients with quiescent disease. Tofacitinib did not modulate the phenotype or function of human intestinal cDC.</div></div><div><h3>Conclussion</h3><div>Tofacitinib does not modulate the phenotype and function of human intestinal cDC in UC. On the contrary, it displays a differential capacity to modulate intestinal monocyte and macrophage phenotype. Future studies should address whether it also translates into a differential function of these cells.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100271"},"PeriodicalIF":4.7,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143176736","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":"The added value of coupling anti-dsDNA and anti-chromatin antibodies in follow-up monitoring of systemic lupus erythematosus patients","authors":"Caroline Carlé ,&nbsp;Françoise Fortenfant ,&nbsp;Chloé Bost ,&nbsp;Julie Belliere ,&nbsp;Stanislas Faguer ,&nbsp;Dominique Chauveau ,&nbsp;Antoine Huart ,&nbsp;David Ribes ,&nbsp;Laurent Alric ,&nbsp;Gregory Pugnet ,&nbsp;Laurent Sailler ,&nbsp;Yves Renaudineau","doi":"10.1016/j.jtauto.2025.100274","DOIUrl":"10.1016/j.jtauto.2025.100274","url":null,"abstract":"<div><h3>Objective</h3><div>The autoimmune response to chromatin (Chr) or one of the nucleosome components (double stranded (ds)DNA and histones) is typically associated with the development of systemic lupus erythematosus (SLE). Related autoantibodies (Ab) are heterogeneous and, among them, anti-dsDNA Ab are part of the classification criteria and recommended for monitoring SLE with regards to lupus flares and therapy responses. However, anti-dsDNA Ab biomarker performances are weak; therefore, coupling anti-dsDNA with anti-Chr Ab can be proposed, which is the aim of this study.</div></div><div><h3>Methods</h3><div>In this single center study from 2009 to 2024, 269 SLE patients with follow-up information were retrospectively selected from a population of 646 individuals, including 325 SLE patients, who tested positive for anti-dsDNA and/or anti-Chr Ab (Bioplex 2200™). Bio-clinical information during follow-up were assessed at several time points through medical records in order to explore associations between the anti-dsDNA/Chr Ab profile with disease presentation, and anti-dsDNA/Chr Ab fluctuations with disease activity using clinical SLEDAI-2K, flares requiring specific treatment, and the therapeutic response.</div></div><div><h3>Results</h3><div>At inclusion in the follow-up analysis, corresponding to diagnosis (116/269, 43.1 %) or flare (153/269, 56.9 %), SLE patients were subdivided into three serological groups: the double positive dsDNA/Chr group (DP+, 190/269: 70.6 %), followed by the single positive Chr group (SP-C+, 42/269: 15.6 %), and the single positive dsDNA group (SP-D+, 37/269: 13.8 %). The DP + group, which presented important anti-dsDNA/Ab variations during follow-up, was at risk to develop lupus nephritis (56.8 % versus 2.4 % in SP-C+ and 29.7 % in SP-D+ groups, p &lt; 0.04) and serositis (30 % versus 9.5 % in SP-C+ group, <em>p</em> = 0.006). During follow-up, anti-dsDNA and Chr Ab levels in the SP-C+ and SP-D+ groups remained stable over time irrespective of disease activity, flares, and therapeutic response. Regarding the DP + group, disease activity was correlated with both anti-dsDNA (RmCorr = 0.46, p = 1.6x110-⁹¹) and anti-Chr (RmCorr = 0.38, p = 2.8x10-⁶⁰) Ab levels, which can be used to predict flares. Following therapy introduction, Ab reduction occurred in all patients from the DP + group with a more pronounced effect reported in complete responders.</div></div><div><h3>Conclusion</h3><div>coupling anti-dsDNA with anti-Chr Ab detection at disease initiation/flare allows definition of endotypes, which is useful to follow disease activity, predict lupus nephritis/serositis, and anticipate therapeutic response in the DP + group.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100274"},"PeriodicalIF":4.7,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143175372","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":"Autoantibodies in systemic sclerosis: From disease bystanders to pathogenic players","authors":"Aurélien Chepy ,&nbsp;Aurore Collet ,&nbsp;David Launay ,&nbsp;Sylvain Dubucquoi ,&nbsp;Vincent Sobanski","doi":"10.1016/j.jtauto.2025.100272","DOIUrl":"10.1016/j.jtauto.2025.100272","url":null,"abstract":"<div><div>Autoantibodies (Aab) are recognized as key indicators in the diagnosis, classification, and monitoring of systemic autoimmune diseases (AID). Recent studies have expanded knowledge through the discovery of new antigenic targets, advanced methods for measuring Aab levels, and understanding their possible pathogenic roles in AID. This narrative review uses systemic sclerosis (SSc) as an example to highlight the importance of Aab associated with HEp-2 immunofluorescence assay positivity (traditionally referred as antinuclear antibodies [ANA]), exploring recent developments in the field. Firstly, we outline the various types of ANA found in SSc and their links with specific disease features. Newly discovered antibodies shed light on SSc cases where Aab had previously gone unidentified. Secondly, we emphasize the necessity for novel quantitative techniques to track Aab levels over time by gathering data regarding the timing of Aab occurrence relative to SSc symptoms and the relationships between Aab concentrations and disease severity. Finally, we discuss the experimental findings suggesting a potential direct role of Aab in the development of SSc. The advancements surrounding Aab provide insights into new disease mechanisms and may lead to innovative diagnostic and treatment approaches.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100272"},"PeriodicalIF":4.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143174952","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":"Monitoring the follow-up of autoimmune chronic atrophic gastritis using parietal cell antibodies and markers of gastric function","authors":"Maria Piera Panozzo ,&nbsp;Antonio Antico ,&nbsp;Nicola Bizzaro","doi":"10.1016/j.jtauto.2025.100273","DOIUrl":"10.1016/j.jtauto.2025.100273","url":null,"abstract":"<div><div>Increased interest in the pathogenesis and the evolution of autoimmune chronic atrophic gastritis (A-CAG) has led to the search for serological markers that can be used to detect changes in the gastric mucosa at an early stage and to monitor the course of the disease. Parietal cell autoantibodies have been proposed as suitable immunological markers of atrophic damage, as they can be detected in the serum when symptoms of gastritis are not yet present. However, the utility of measuring only the level of parietal cell autoantibodies in the follow-up of A-CAG does not appear to suffice. Recent evidence has suggested that, in monitoring A-CAG, parietal cell antibodies should be associated with an evaluation of gastric function through biochemical and hormonal tests, such as pepsinogens and gastrin 17. This integrated approach will allow for the more effective real-time monitoring of the state of the gastric mucosa. As A-CAG is a progressive disorder associated with an increased risk of gastric cancer and neuroendocrine tumors, the precise follow-up of patients with gastric atrophy needs to be better defined. Further longitudinal studies in large cohorts must be performed with long-term follow-up.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"10 ","pages":"Article 100273"},"PeriodicalIF":4.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143174995","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}