Journal of Translational Autoimmunity最新文献

{"title":"Systemic lupus pregnancies are characterized by an intrinsic pro-inflammatory monocyte transcriptome, driven by an aberrant miRNA signature","authors":"Marc Scherlinger ,&nbsp;Eloi Schmauch ,&nbsp;Raphaël Carapito ,&nbsp;Angélique Pichot ,&nbsp;Ghada Alsaleh ,&nbsp;Nicodème Paul ,&nbsp;Anne Molitor ,&nbsp;François Lefebvre ,&nbsp;Catherine Schmidt-Mutter ,&nbsp;Seiamak Bahram ,&nbsp;Jean Sibilia ,&nbsp;Philippe Georgel","doi":"10.1016/j.jtauto.2025.100347","DOIUrl":"10.1016/j.jtauto.2025.100347","url":null,"abstract":"<div><h3>Objective</h3><div>Pregnancy induces profound immunological adaptations that usually promote tolerance and reduce autoimmune activity. However, women with systemic lupus erythematosus (SLE) remain at increased risk of disease flares and pregnancy complications, whereas rheumatoid arthritis (RA) often improves during gestation. To better understand this divergence, we longitudinally characterized transcriptomic and microRNA (miRNA) changes in circulating monocytes from healthy, RA, and SLE pregnancies.</div></div><div><h3>Methods</h3><div>Pregnant women with SLE (n = 5), RA (n = 4), and healthy controls (n = 5) were followed from preconception to three months postpartum. CD14⁺ monocytes were isolated at each visit and profiled using RNA sequencing and miRNA sequencing. Differential expression analyses were performed using DESeq2, modelling patient ID as a covariate. Pathway enrichment and upstream regulator analyses were conducted using Ingenuity Pathway Analysis and Reactome. Correlation-based miRNA–mRNA regulatory networks were inferred using miRTarBase-validated interactions.</div></div><div><h3>Results</h3><div>Healthy and RA pregnancies exhibited a shift toward an alternatively activated (anti-inflammatory) monocyte phenotype, characterized by downregulation of TNF, IFN-γ, and IL-1 signalling pathways. In contrast, SLE pregnancies maintained a persistent M1-like (pro-inflammatory) program throughout gestation and postpartum, independent of clinical flare status. miRNA profiling revealed selective downregulation of miR-106a-5p and miR-148b-5p in SLE monocytes, accompanied by enrichment of cytokine-related pathways among their predicted targets. These dysregulated miRNAs were linked to activation of immune pathways including IL-12 signalling, interferon responses, apoptosis, and complement activation.</div></div><div><h3>Conclusion</h3><div>SLE pregnancies are characterized by a failure to achieve monocyte immunotolerance, driven in part by aberrant miRNA regulation. These findings highlight molecular mechanisms underlying persistent inflammation in SLE pregnancy and identify candidate transcriptomic and miRNA biomarkers that may support future risk stratification or therapeutic modulation.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100347"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926253","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":"Data-driven classification of primary Sjögren’s syndrome: From cluster analysis to clinical immune phenotypes and predictive biomarkers","authors":"Jianbin Li ,&nbsp;Suiran Li ,&nbsp;Wei Liu","doi":"10.1016/j.jtauto.2025.100338","DOIUrl":"10.1016/j.jtauto.2025.100338","url":null,"abstract":"<div><h3>Background</h3><div>Primary Sjögren’s Syndrome (pSS) exhibits significant clinical heterogeneity, and traditional organ-based classification systems fail to capture the underlying disease mechanisms. This study aims to identify distinct clinical immune phenotypes of pSS through a data-driven approach and explore their predictive biomarkers.</div></div><div><h3>Method</h3><div>This cross-sectional study included 1087 patients who met the 2016 ACR/EULAR classification criteria for primary Sjögren’s syndrome between 2014 and 2024. Unsupervised K-means clustering analysis was applied to 10 organ involvement variables to identify natural patient subgroups. Network analysis was used to explore the associations between organ involvement and laboratory biomarkers. Multivariable logistic regression was employed to identify independent predictors of subgroup assignment, and restricted cubic spline analysis was conducted to assess the nonlinear relationships between key biomarkers and subtype risk.</div></div><div><h3>Results</h3><div>Clustering analysis identified two distinct phenotypes: Phenotype 1 (multi-system inflammatory subtype, n = 594) was characterized by widespread musculoskeletal involvement (100 %) and significantly elevated inflammatory markers (RF: 246.41 ± 1177.49 vs 32.75 ± 126.74 IU/mL, P &lt; 0.001); Phenotype 2 (glandular-limited high immunoglobulin subtype, n = 493) was primarily characterized by glandular involvement (40.7 %), higher IgG levels, and less systemic involvement. Network analysis revealed a strong correlation between RF and musculoskeletal involvement (r = 0.32, P &lt; 0.001). Independent predictors of Phenotype 1 included male gender (OR 2.559, 95 % CI 1.109–6.090), elevated potassium (OR 1.607, 95 % CI 1.061–2.433), and elevated RF levels (OR 1.004, 95 % CI 1.002–1.005). A composite clinical prediction score incorporating these biomarkers achieved an AUC of 0.717 (95 % CI: 0.684–0.751) for phenotype discrimination. Nonlinear analysis showed complex U-shaped and inverted U-shaped relationships between key biomarkers and phenotype risk.</div></div><div><h3>Conclusion</h3><div>pSS consists of distinct clinical phenotypes with varying pathophysiological characteristics. The data-driven classification system complements traditional severity grading and provides new insights into precision medicine approaches. RF is a key biomarker linking musculoskeletal manifestations with the severity of systemic inflammation and may serve as an important indicator for precise subtyping and targeted therapy.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100338"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683687","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":"Decoding ulcerative colitis pathogenesis through transcriptomics: from dysregulated gene networks to targeted intervention strategies","authors":"Xiang Zhu ,&nbsp;Yujie Yang ,&nbsp;Yi Zhu","doi":"10.1016/j.jtauto.2025.100334","DOIUrl":"10.1016/j.jtauto.2025.100334","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;div&gt;Ulcerative colitis (UC) is an immune-mediated chronic inflammatory bowel disease, and with the rising global incidence and the risk of malignant transformation, the treatment of UC is challenged by heterogeneous progression and limited targeted therapies, and its underlying pathogenesis remains unclear. This study aims to identify novel therapeutic targets for UC, elucidate the genetic factors associated with UC development, and advance precision medicine strategies for UC.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Differential expression analysis was performed on three independent UC datasets from the Gene Expression Omnibus (GEO) database, identifying differentially expressed genes (DEGs) associated with UC. An eQTL-MR analysis was conducted to identify UC-related gene expression loci, and the results were intersected with the GEO differential analysis using a Venn diagram. Subsequently, a protein-protein interaction network was constructed based on the 20 intersecting genes identified through both eQTL-MR and differential expression analysis, using STRING. Key hub genes were then identified based on centrality scores calculated in Cytoscape. Additionally, Gene Set Enrichment Analysis (GSEA) and Gene Ontology (GO)/Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were used to explore the functional roles and pathways of these genes. Finally, the results obtained for the target genes were validated.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Twenty intersecting genes were identified, specifically PITPNC1, OLFM1, PARP9, BATF2, PDGFRB, LEF1, CST7, HCLS1, SLC16A6, CCR7, KMO, ITGA4, SLC22A5, ASB13, SLC22A4, DNMBP, PGAP3, FAAH, SLC7A9, and BTNL8. These genes are involved in fundamental biological processes and pathways, including immune response modulation and epithelial barrier regulation. Additionally, CIBERSORT analysis revealed a unique immune cell distribution in UC and highlighted the association between immune cells and the intersecting genes. Gene Set Enrichment Analysis (GSEA) showed that high expression levels of HCLS1, ITGA4, and PDGFRB may collectively contribute to the recruitment and activation of inflammatory cells, as well as the amplification of immune signaling. Conversely, lower expression levels of these genes suggest that the tissue may be in a state of reduced inflammation or repair. The MR analysis was consistent with the results of variance analysis in the validation cohort, further reinforcing the reliability of our MR findings.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusions&lt;/h3&gt;&lt;div&gt;HCLS1, ITGA4, and PDGFRB may represent core modules involved in T/B cell homing and activation, pro-inflammatory macrophage recruitment, and extracellular matrix responses. These genes interact with upregulated genes to promote the amplification of inflammation, counteracting with downregulated metabolic-related genes. Together, they contribute to the molecular foundation of the inflammatory and metabolic protective phenotype ","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100334"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145738290","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":"Type I interferon-dependent and -independent signaling underlie autoantibody production in a murine lupus model","authors":"Jerrold S. Levine ,&nbsp;Céleste Pilon ,&nbsp;Rebecca Subang ,&nbsp;David Salem ,&nbsp;Elena Lonina ,&nbsp;Salman T. Qureshi ,&nbsp;Gregory J. Fonseca ,&nbsp;Philippe Gros ,&nbsp;Joyce Rauch","doi":"10.1016/j.jtauto.2026.100351","DOIUrl":"10.1016/j.jtauto.2026.100351","url":null,"abstract":"<div><div>Systemic lupus erythematosus (SLE) is characterized by the development of autoantibodies against diverse self-antigens and damage to multiple organs. Immunization with the SLE autoantigen β2-glycoprotein I and lipopolysaccharide (LPS) induces a murine model of SLE with the sequential emergence of multiple hallmark SLE autoantibodies. LPS is a TLR4 trigger of innate immunity and inflammation that signals through adaptor proteins MyD88 and TRIF, resulting in the production of both inflammatory cytokines and type I interferons (IFN-I). We hypothesized that both IFN-I-dependent and -independent mechanisms are important in the initiation of SLE. Using our induced murine model of SLE, we found that TRIF deficiency completely abrogated autoantibody production. Downstream of TRIF, both IRF3 and IFNaR (IFN-I receptor) deficiency significantly diminished autoantibody production. Using transcriptomics, we identified 27 upregulated and 4 downregulated TRIF- and IRF3-dependent genes differentially expressed by both dendritic cells (DCs) and macrophages upon induction of the SLE model. While most genes were dependent on IFN-I signalling, some showed little or no IFN-I dependence. Notably, the 27 upregulated genes correlated with published datasets for human SLE. Our findings map the transcriptional response of macrophages and DCs early during pathogenesis of SLE, including pathways associated with both IFN-I-dependent and -independent genes in SLE. Investigation of candidate genes within both gene subsets may provide insight into the events leading up to SLE as well as potential therapeutic targets.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100351"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173458","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":"Upregulated GLUT1 expression correlates with type I interferon activity and disease severity in cutaneous lupus erythematosus","authors":"Laura Anna Bokor ,&nbsp;Botond L. Szabolcs ,&nbsp;Zsófia Király ,&nbsp;Anita Mohos ,&nbsp;Ágota Szepesi ,&nbsp;Viktória Varga ,&nbsp;Anna Sebestyén ,&nbsp;Lajos V. Kemény ,&nbsp;Péter Holló ,&nbsp;Bernadett Hidvégi","doi":"10.1016/j.jtauto.2026.100375","DOIUrl":"10.1016/j.jtauto.2026.100375","url":null,"abstract":"<div><h3>Background</h3><div>The pathogenesis of cutaneous lupus erythematosus (CLE) is driven by the overactivation of the type I interferon (IFN-I) system. Although dysregulated glucose metabolism has been implicated in autoimmune inflammation, its role in CLE remains largely unexplored. This study aims to elucidate the role of glucose metabolism in CLE, specifically exploring its correlation with IFN-I activity and its contribution to disease severity.</div></div><div><h3>Methods</h3><div>Skin biopsies were obtained from 51 patients with active, untreated CLE — including two of its most prevalent subtypes: 26 with subacute cutaneous lupus erythematosus (SCLE) and 25 with discoid lupus erythematosus (DLE) — and 8 healthy controls. Glucose uptake and IFN-I system activation was evaluated via GLUT1 (SLC2A1) and MxA (MX1) immunohistochemistry, respectively. Disease activity was measured using the CLASI-A score. Publicly available transcriptomic datasets were analyzed using Spearman's rank correlation to evaluate the association between <em>SLC2A1</em> and <em>MX1</em> mRNA levels.</div></div><div><h3>Results</h3><div>GLUT1 expression was significantly increased in both CLE subtypes compared to healthy controls (SCLE: p = 0.0344, DLE: p = 0.0356). MxA expression in keratinocytes and lymphocytes was also markedly elevated in CLE samples (p = 0.0031, p = 0.0059). Keratinocyte GLUT1 expression positively correlated with keratinocyte and lymphocyte MxA expression (p = 0.003, r = 0.41; p &lt; 0.001, r = 0.483) and with CLASI-A scores (p &lt; 0.001, r = 0.47). Additionally, a significant positive correlation was observed between <em>SLC2A1</em> and <em>MX1</em> mRNA expression across multiple cell lines.</div></div><div><h3>Conclusion</h3><div>Our findings identify a link between elevated GLUT1 expression, IFN-I pathway activation, and CLE disease activity, suggesting that enhanced glucose metabolism may contribute to the immunopathogenesis and clinical severity of CLE.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100375"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148184131","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":"Serum pepsinogen Ⅰ and the pepsinogen Ⅰ/Ⅱ ratio as a non-invasive predictive marker for autoimmune metaplastic atrophic gastritis","authors":"Chuyan Chen,&nbsp;Fandong Meng,&nbsp;Linlin Shao,&nbsp;Shutian Zhang,&nbsp;Peng Li,&nbsp;Haiyi Hu","doi":"10.1016/j.jtauto.2026.100377","DOIUrl":"10.1016/j.jtauto.2026.100377","url":null,"abstract":"<div><h3>Objective</h3><div>Autoimmune metaplastic atrophic gastritis (AMAG) is a chronic inflammatory disease characterized by autoimmune destruction of parietal cells, causing profound gastric body and fundus atrophy. AMAG is frequently overlooked or misdiagnosed in clinical practice. This study aimed to identify optimal cut-off values for serum pepsinogens (PGs) as a non-invasive diagnostic tool for AMAG in a retrospective cohort.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed the clinical and laboratory data of 520 AMAG patients from our center and compared them with those of 223 control patients who underwent serum PG testing and esophagogastroduodenoscopy (EGD) for various indications during the same period.</div></div><div><h3>Results</h3><div>The AMAG cohort demonstrated a marked female predominance compared with controls (74.6% vs. 45.2%, p &lt; 0.001), and 23.1% of patients were asymptomatic at diagnosis. Serological profiling showed that anti-parietal cell antibody was positive in 65.9% (309/469) of tested individuals, while anti-intrinsic factor antibody was detected in 39.1% (61/156). Gastric neuroendocrine tumors (NETs) were the most frequent neoplastic finding in AMAG (105 patients, 20.2%). Fasting gastrin-17 levels were significantly elevated in AMAG patients alongside markedly decreased pepsinogen I (PG I) and PG I/II ratio compared with controls (all p &lt; 0.001). Receiver operating characteristic analysis identified PG I &lt; 22.45 ng/mL (AUC: 0.964, 95% CI: 0.950–0.978; sensitivity: 88.9%, specificity: 96.0%) and PG I/II ratio &lt;2.25 (AUC: 0.957, 95% CI: 0.941–0.974; sensitivity: 89.6%, specificity: 95.1%) as optimal cut-offs for distinguishing AMAG from controls. The combined use of PG I &lt; 22.45 ng/mL and PG I/II ratio &lt;2.25 achieved a specificity of 97.3% (95% CI: 94.2%–99.0%).</div></div><div><h3>Conclusions</h3><div>Serum PG I and the PG I/II ratio demonstrate good diagnostic performance for AMAG, with high specificity in particular. These biomarkers may serve as a useful non-invasive screening tool for AMAG.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100377"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148230940","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":"Immunoprotective and neuroprotective properties of gut microbiome in psoriasis","authors":"Amirhesan Yahyapour ,&nbsp;Ali Najafi ,&nbsp;Ali Ahmadi ,&nbsp;Navvabeh Salarizadeh","doi":"10.1016/j.jtauto.2026.100348","DOIUrl":"10.1016/j.jtauto.2026.100348","url":null,"abstract":"<div><div>Psoriasis impacts nearly 100 million people globally and is associated with neuropsychiatric comorbidities such as depression and anxiety. With gut microbiome dysbiosis serving as a primary pathophysiological factor, the gut-brain-skin axis provides a crucial framework for understanding this relationship. This review evaluates the mechanisms of the gut-brain-skin axis in psoriasis pathophysiology and assesses the therapeutic potential of microbiome-based treatments, combining preclinical, clinical, and multi-omics data. Patients with psoriasis show specific gut dysbiosis patterns, including reduced microbial diversity, lower SCFA-producing bacteria (especially Faecalibacterium and Akkermansia), and increased pro-inflammatory bacteria. This microbial imbalance damages intestinal barrier integrity, triggers systemic inflammation, activates cutaneous Th17 pathways, and induces neuroinflammation through blood-brain barrier disruption. Axis communication occurs through immune-inflammatory mechanisms mediated by SCFAs and neuroendocrine pathways involving microbially-derived neurotransmitters (GABA, serotonin, dopamine). Metagenomic research indicates functional deficiencies in neurotransmitter and SCFA synthesis pathways are more significant than taxonomic alterations. Machine learning models can utilize these functional features to identify patients at risk for neuropsychiatric comorbidities and predict treatment response. Recent randomized controlled trials demonstrate that targeted interventions (probiotics, prebiotics, postbiotics, fecal microbiota transplantation) significantly improve Psoriasis Area and Severity Index scores, inflammatory markers, and microbiota composition. The evidence supports a shift toward integrated microbiome strategies, emphasizing functional approaches including mitochondrial therapies, psychobiotics, precision nutrition, and multi-omics-guided therapies.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100348"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926255","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":"“CANDLE syndrome: A closer look at a rare autoinflammatory disorder”","authors":"Shivam Singh,&nbsp;Ashish Kumar Sharma","doi":"10.1016/j.jtauto.2025.100339","DOIUrl":"10.1016/j.jtauto.2025.100339","url":null,"abstract":"<div><div>A newly identified autoinflammatory condition called CANDLE syndrome (chronic atypical neutrophilic dermatosis with lipodystrophy and increased temperature) is characterized by early onset, recurring fever, skin lesions, and multisystemic inflammatory symptoms. It has been demonstrated that the majority of patients had PSMB8 gene mutations. It leads to dysfunction in the proteasome/immunoproteasome system and subsequent overproduction of type 1 interferons. Patients usually exhibit lipodystrophy, fever, rashes on the skin, and malnutrition in the early stages of infancy. The results of skin biopsies, laboratory tests, and clinical symptoms all support the diagnosis of CANDLE syndrome. Although there isn't a specific treatment for CANDLE syndrome, JAK inhibitors like baricitinib have demonstrated some effectiveness in treating its symptoms. For CANDLE syndrome patients to receive the right therapeutic interventions, early diagnosis and molecular testing are essential. A positive interferon signature has also been found to be a diagnostic indicator for the condition. Although there are no particular treatments for CANDLE syndrome, research is still being done to determine how well immunosuppressive medications, biological agents, and glucocorticoids work in treating the condition. Current research generally aims to improve the quality of life for individuals with CANDLE syndrome through the development of targeted medications, the elucidation of genetic determinants, and the advancement of diagnostic methods.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100339"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145738292","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":"Exploring the immunomodulatory effects of environmental contaminants on autoimmune patients: An in vitro approach","authors":"Yeny Acosta-Ampudia ,&nbsp;Diana M. Monsalve ,&nbsp;Daniel Galeano-Sánchez ,&nbsp;Manuel Rojas ,&nbsp;Carolina Ramírez-Santana","doi":"10.1016/j.jtauto.2025.100341","DOIUrl":"10.1016/j.jtauto.2025.100341","url":null,"abstract":"<div><h3>Background</h3><div>Autoimmune diseases are multifactorial, with environmental contaminants increasingly recognized as risk factors. This pilot study investigated the <em>in vitro</em> effects of particulate matter (PM), silica, and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on peripheral blood mononuclear cells (PBMCs) from healthy donors (HD) and patients with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE).</div></div><div><h3>Methods</h3><div>PBMCs were obtained from HD (n = 6), RA patients (n = 5), and SLE patients (n = 5) and stimulated for 24 h with PM (100 μg/mL), silica (30 μg/mL), or TCDD (250 pg/mL). Immunophenotyping by flow cytometry was performed in HD, characterizing T cell subsets, B cells, NK/NKT cells, monocytes, and dendritic cells, including activation markers. Production of 18 cytokines and chemokines was quantified in all groups using Cytometric Bead Array. Activation of intracellular signaling pathways (AKT, NFκB, p38 MAPK, STAT1, STAT3) was assessed by Western blot.</div></div><div><h3>Results</h3><div>All contaminants induced strong immune activation. In HD, flow cytometry revealed strong activation of monocytes and dendritic cells, with increased co-stimulatory markers (CD40, CD80, CD83) and skewing of T cells toward effector phenotypes. Cytokine analysis showed substantial overlap in inflammatory profiles across HD, RA, and SLE, despite the significant upregulation of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), growth factors (GM-CSF, G-CSF), and regulatory cytokines (IL-10). Western blot confirmed modulation of signaling pathways, with PM notably enhancing p38 MAPK phosphorylation in HD and RA.</div></div><div><h3>Conclusion</h3><div>Environmental contaminants elicit robust immunomodulatory effects in PBMCs. The overlap in cytokine profiles and signaling responses across HD, RA, and SLE indicates a highly conserved cellular response to environmental stressors, independent of autoimmune disease status.</div></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100341"},"PeriodicalIF":3.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145738291","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":"Corrigendum to “Data-driven classification of primary Sjögren's syndrome: From cluster analysis to clinical immune phenotypes and predictive biomarkers” [J. Transl. Autoimmun. 12 (2026) 100338]","authors":"Jianbin Li,&nbsp;Suiran Li,&nbsp;Wei Liu","doi":"10.1016/j.jtauto.2025.100343","DOIUrl":"10.1016/j.jtauto.2025.100343","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":"12 ","pages":"Article 100343"},"PeriodicalIF":3.8,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13294866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148346452","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}