European Journal of Immunology最新文献

{"title":"The Mitigating Effect of Combined Glucocorticoids with Immune Checkpoint Inhibitors on Lymphocyte Activation Gene-3 and Programmed Death-1 Expression","authors":"Smadar Gertel,&nbsp;Ari Polachek,&nbsp;Victoria Furer,&nbsp;Tali Ofir Dovrat,&nbsp;Chen Avaky,&nbsp;Adi Broyde,&nbsp;Hila Nochimovitz,&nbsp;Ori Elkayam","doi":"10.1002/eji.70033","DOIUrl":"https://doi.org/10.1002/eji.70033","url":null,"abstract":"<p>Cancer immunotherapy with immune checkpoint inhibitors (ICI) shows promising therapeutic efficacy but can cause immune-related adverse events (irAEs). Glucocorticoids (GCs) are commonly employed with ICI to mitigate irAEs. We had found previously that GCs upregulate significantly the inhibitory molecule, lymphocyte activation gene-3 (LAG-3) in peripheral blood and synovial fluid mononuclear cells (PBMCs and SFMCs, respectively). Here, we investigated the effect of GCs combined with ICI on LAG-3 and programmed death-1 (PD-1) expression in SFMCs of 32 inflammatory arthritis patients and PBMCs of 15 healthy controls. GC+Pembrolizumab (PEM, anti-PD-1) induced IL-10 and suppressed IFN-γ, TNF-α, and IL-17A mRNA expressions compared with PEM alone in PBMCs and SFMCs. PBMC proliferation was markedly inhibited by GC+PEM (3.5 ± 0.7%, <i>p </i>&lt; 0.0006) compared with PEM alone (26.2 ± 6.5%). GC+PEM increased the CD4⁺LAG-3⁺ T cells (4.9±1.2%, <i>p </i>&lt; 0.03) compared with PEM alone (0.9 ± 0.3%), but did not affect CD4⁺PD-1⁺ T cells. The effect of the drugs on synovial cells revealed that GC+PEM remarkably increased the CD14⁺LAG-3⁺ cells in SFMCs (10.4 ± 2.0%, <i>p </i>&lt; 0.0001) compared with PEM alone (0.6 ± 0.2%), but not the CD14⁺PD-1⁺ cells. Thus, GC combined with ICI might exhibit contrasting activity via upregulation of CD4⁺LAG-3⁺ T and CD14⁺LAG-3⁺ cells in circulation and synovial milieu, respectively, possibly interfering with the ICI activity.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70033","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144814676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Collaborative Special Issue: Highlights from the Belgian–Dutch Immunology Meeting","authors":"Melissa M. J. van Gool,&nbsp;Hind Hussein,&nbsp;Anissa Zouzaf,&nbsp;Farahnaz Rayatdoost","doi":"10.1002/eji.70030","DOIUrl":"https://doi.org/10.1002/eji.70030","url":null,"abstract":"<p>On November 21–22, 2023, the third Joint Belgian–Dutch Immunology Meeting took place at the Flanders Meeting &amp; Convention Center in Antwerp, Belgium. This event brought together over 700 researchers and clinicians from across the Netherlands and Belgium to exchange the latest insights in fundamental and translational immunology. Co-organized by the Belgian Immunological Society (BIS) and the Dutch Society for Immunology (NVVI), the meeting featured keynote lectures from international leaders in the field, including Prof. Manfred Kopf, Prof. Donna Farber, Dr. Julie Déchanet-Merville, and Prof. Georg Schett. The scientific program also included thematic parallel sessions with selected abstract presentations, poster sessions, and a dedicated Young Investigators session to highlight the work of early-career scientists. Building on the legacy of previous joint BIS–NVVI meetings held in 1988 and 2002, the 2023 edition marked a renewed commitment to cross-border collaboration and the exchange of scientific ideas between the Belgian and Dutch immunology communities.</p><p>The Belgian–Dutch Immunology Highlights special issue, inspired by the 2023 Joint Belgian–Dutch Immunology Meeting, features 20 selected original research and review articles, reflecting the scientific diversity and depth of topics presented at the meeting from fundamental insights into infection and inflammation to advances in immune regulation and emerging therapeutic strategies. Among these, we especially highlight seven articles from first-time authors: five by first-time first authors and two by first-time corresponding authors. For many of them, this marks an important milestone in their scientific careers.</p><p>Innate immune responses are not only regulated by external cues but are also modulated by sophisticated internal systems, which ensure an adequate balance between activation and suppression to preserve systemic homeostasis as well as tissue integrity.</p><p>Koops &amp; Meyaard [<span>1</span>] review a lesser-known yet crucial inhibitory checkpoint in myeloid cells: the inhibitory receptor VSTM1/SIRL-1. As a pattern recognition receptor with an inhibitory function, VSTM1 suppresses the production of reactive oxygen species (ROS) and the formation of neutrophil extracellular traps (NETs) in response to both host and microbial ligands, including LL37, S100, and bacterial phenol-soluble modulins (PSMs). Its function highlights the importance of active immune dampening mechanisms, especially in contexts where the presence of pathogens does not necessitate the involvement of immune cells, such as in the skin and gut.</p><p>Parallel to this, Biscu et al. [<span>2</span>] illustrate how environmental cues, including dietary inputs such as vitamins and iron, microbial metabolites, and local tissue factors, shape macrophage function via metabolic rewiring. This plasticity supports both inflammatory and reparative programs and is central to the concept of macrophage niches. ","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70030","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144810978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Meet the Brightest in Immunology: Q&A With Award-Winning Researchers From the 2023 BIS-NVVI Annual Meeting","authors":"Melissa M.J. van Gool,&nbsp;Hind Hussein,&nbsp;Anissa Zouzaf,&nbsp;Farahnaz Rayatdoost,&nbsp;Ernesto Rodriguez,&nbsp;Leslie Naesens,&nbsp;Linde Meyaard","doi":"10.1002/eji.70029","DOIUrl":"https://doi.org/10.1002/eji.70029","url":null,"abstract":"","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144810977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current and Emerging Autoantibodies in Ulcerative Colitis","authors":"Erick A. Mendieta-Escalante,&nbsp;Klaas Nico Faber,&nbsp;Gerard Dijkstra","doi":"10.1002/eji.202451721","DOIUrl":"https://doi.org/10.1002/eji.202451721","url":null,"abstract":"<p>Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by immune dysregulation and epithelial barrier dysfunction. Circulating autoantibodies have been observed in many patients, suggesting a role in disease pathogenesis and progression. Atypical anti-neutrophil cytoplasmic antibodies (a-ANCAs), anti-goblet cell antibodies (GAB), and anti-integrin αvβ6 antibodies have emerged as promising biomarkers for UC diagnosis, disease monitoring, and therapeutic response prediction. a-ANCAs are detected in up to 80% of UC patients, but their precise antigenic targets remain unclear. Evidence suggests their reactivity may involve neutrophil extracellular traps (NETs) and DNA–protein complexes, distinguishing them from ANCAs in vasculitis. GAB may contribute to mucus layer depletion and epithelial dysfunction. Anti-integrin αvβ6 antibodies have demonstrated high specificity for UC related to disease severity and potential for early detection.</p><p>Despite the diagnostic potential of these autoantibodies, lack of standardization, variability in detection methods, unclear binding sites, and lack of relevant clinical studies limit their use in clinical practice. Advances in epitope mapping, flow cytometry, and high-throughput immunoassays are promising approaches. We review the role of these autoantibodies in UC pathogenesis, highlight recent developments, and discuss their potential as biomarkers for improving diagnosis, disease monitoring, and personalized treatment strategies for UC patients.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.202451721","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of Regulatory T Cells From Human Memory CD4+T Cells by Upregulation of Naked Cuticle Homolog 2","authors":"Jiajun He,&nbsp;Kristy Ou,&nbsp;Michael Schmueck-Henneresse,&nbsp;Edgar Specker,&nbsp;Jérôme Paul,&nbsp;Marc Nazare,&nbsp;Jens Peter von Kries,&nbsp;Julia K. Polansky,&nbsp;Alf Hamann,&nbsp;Stefan Frischbutter","doi":"10.1002/eji.70018","DOIUrl":"https://doi.org/10.1002/eji.70018","url":null,"abstract":"<p>Regulatory T cells are indispensable for immune homeostasis and tolerance to self-antigens and allergens. The imbalance between immune responses and tolerance causes allergic and autoimmune diseases. A promising therapeutic strategy is to support immune tolerance by converting conventional T cells into suppressive regulatory T cells with small molecular weight compounds, an area that is underexplored. Here, we report the identification, characterization, and validation of a novel quinoxaline derivative (IFA005) that converts human memory CD4⁺T cells into suppressive Foxp3-expressing Tregs in vitro. Mechanistically, IFA005 regulated the expression of naked cuticle homolog 2 and impaired the phosphorylation of glycogen synthase kinase-3β, which led to the degradation of β-catenin and thus blocked the Wnt-β-catenin pathway. Our findings indicate that IFA005 could be a promising candidate for inducing immune tolerance by converting effector T cells into suppressive Treg cells through the inhibition of the Wnt-β-catenin pathway.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70018","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Aspirin Challenge on Innate Lymphoid Cells in Asthma Patients With Aspirin Hypersensitivity","authors":"Radosław Kacorzyk,&nbsp;Bogdan Jakiela,&nbsp;Alicja Maciejska,&nbsp;Agnieszka S. Węgrzyn,&nbsp;Adam Ćmiel,&nbsp;Marek Sanak,&nbsp;Lucyna Mastalerz","doi":"10.1002/eji.70020","DOIUrl":"https://doi.org/10.1002/eji.70020","url":null,"abstract":"<p>Previous studies confirmed increased group 2 innate lymphoid cell (ILC2s) count in nasal scrapings, alongside a reduced blood ILC2 count, in patients with nonsteroidal anti-inflammatory drug-exacerbated respiratory disease (N-ERD) after intranasal administration of cyclooxygenase-1 inhibitors. This study aimed to assess the role of blood and sputum ILCs in N-ERD patients during oral aspirin-induced bronchospasm and to compare patients with eosinophilic and noneosinophilic airway inflammatory phenotypes of asthma. Induced sputum, blood, and urine samples were collected in 24 patients with confirmed N-ERD at baseline and during aspirin-induced bronchospasm. Sputum and blood ILC counts were evaluated using flow cytometry. There was a significant increase in blood ILC1 count (<i>p </i>&lt; 0.001) and percentage (<i>p</i> = 0.003) during aspirin-induced bronchospasm. No significant changes in sputum ILCs were observed, but the number of detected ILCs was very low. There was a significant reduction in induced sputum supernatant (ISS) levels of prostaglandins PGE₂ (<i>p</i> = 0.004) and PGD₂ (<i>p</i> = 0.045), leukotriene B₄ (<i>p</i> = 0.045), and 15-oxo-eicosatetraenoic acid (<i>p</i> = 0.045) during aspirin-induced bronchospasm. Blood ILC1 count is increased during oral aspirin-induced bronchospasm in patients with N-ERD, but sputum ILC count at baseline is very low. Therefore, no reliable changes in sputum ILC counts can be detected during bronchospasm.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70020","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PD-L2 Inhibits Protective Immunity, Th2 Cell Functional Quality, and GATA-3 Expression During Filarial Nematode Infection","authors":"Johanna A. Knipper,&nbsp;Sharon M. Campbell,&nbsp;Judith E. Allen,&nbsp;Matthew D. Taylor","doi":"10.1002/eji.70021","DOIUrl":"https://doi.org/10.1002/eji.70021","url":null,"abstract":"<p>Filarial nematodes infect over 200 million people, predominantly stimulating a Type 2 immune response. Protective immunity takes decades to become effective due to dominant immune suppression that develops during infection. Using <i>Litomosoides sigmodontis</i> infection as a murine model of filariasis, we previously demonstrated that PD-1 co-inhibition causes Th2 cells to become intrinsically dysfunctional or hypo-responsive during infection, resulting in impaired protective immunity. Τhis study demonstrates that Th2 cell-intrinsic hypo-responsiveness is associated with a loss of GATA-3 expression by CD4⁺ T cells from WT, but not PD-L2^−/− mice. PD-L2^−/− mice were more resistant to <i>L. sigmodontis</i> and had increased Th2 cell-intrinsic functional quality. CD19⁺ B cells expressed PD-L2, and Jh^−/− B cell-deficient mice were more resistant to infection. However, Th2 cell-intrinsic hypo-responsiveness still developed in Jh^−/− mice, and restricting PD-L2 deficiency to B cells using bone marrow chimaeras did not alter resistance to <i>L. sigmodontis</i> or Th2 cell-intrinsic functional quality. Together, these data indicate that PD-L2 inhibits protective immunity to <i>L. sigmodontis</i>, downregulates GATA-3 in CD4⁺ T cells, and induces Th2 cell-intrinsic hypo-responsiveness. Whilst B cells play a suppressive role during infection, this is independent of PD-L2 and B cells do not instigate Th2 cell-intrinsic hypo-responsiveness.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD8 T Cell Hyperfunction and Reduced Tumour Control in Murine Models of Advanced Liver Disease","authors":"Jood Madani,&nbsp;Jiafeng Li,&nbsp;Ma. Enrica Angela Ching,&nbsp;Agatha Vranjkovic,&nbsp;Katrina Jorritsma,&nbsp;Mohamed S. Hasim,&nbsp;Manijeh Daneshmand,&nbsp;Natasha Campeau,&nbsp;David A. Lawton,&nbsp;Salman Bagheri,&nbsp;Angela C. Cheung,&nbsp;Erin E. Mulvihill,&nbsp;Jennifer E. Bruin,&nbsp;Michele Ardolino,&nbsp;Angela M. Crawley","doi":"10.1002/eji.70026","DOIUrl":"https://doi.org/10.1002/eji.70026","url":null,"abstract":"<p>Immune dysfunction in liver disease contributes to significant morbidities, depending on liver damage severity and aetiology. We previously reported long-lasting generalized CD8 T cell hyperfunction in chronic HCV infection with advanced fibrosis, yet its separation from viral and fibrosis-driven effects, as well as clinical outcomes of advanced fibrosis, remains unclear. In a murine model of carbon tetrachloride-induced progressive liver fibrosis, advanced fibrosis was observed by 12 weeks, with pathologies similar to those of human chronic HCV infection. Blood-circulating CD8 T cells showed IFN-γ and granzyme B (GrB) hyperfunction in response to anti-CD3/28 stimulation, as well as impaired responses to ectopic tumour challenge and anti-PD-1/CTLA-4 immunotherapy. Hyperfunction and impaired tumour responses were retained despite liver insult cessation. In a 45% HFD model, which induced steatosis and minimal fibrosis, IFN-γ and GrB hyperfunction was also observed in blood-circulating CD8 T cells. This study highlights a prolonged systemic CD8 T cell dysfunction acquired during progressive liver disease, associated with impaired antitumour and immunotherapy responses. These mirror the bulk CD8 T cell dysfunction observed in advanced liver diseases in humans, suggesting that these models could be valuable for future mechanistic studies aimed at identifying targets to help improve clinical outcomes in chronic liver disease.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Testosterone Suppresses IL-17 Expression by Targeting RORγt Functions","authors":"Akshay Binayke,&nbsp;Rajdeep Dalal,&nbsp;Charu Suri,&nbsp;Jyotsna Dandotiya,&nbsp;Srikanth Sadhu,&nbsp;Yashwant Kumar,&nbsp;Shailendra Asthana,&nbsp;Deepak Kumar Rathore,&nbsp;Amit Awasthi","doi":"10.1002/eji.70016","DOIUrl":"https://doi.org/10.1002/eji.70016","url":null,"abstract":"<div>\u0000 \u0000 <p>Th17 cells play a crucial role in autoimmune disease pathogenesis. However, the mechanisms behind the sex differences in immune responses, particularly women's higher susceptibility to autoimmune diseases, remain unclear. This study investigated the role of testosterone in modulating the IL-17 response. IL-17 levels and IL-17-expressing cells were compared between males and females, and testosterone's effect on Th17 differentiation was evaluated. In an imiquimod-induced psoriasis mouse model, testosterone supplementation reduced psoriasis severity in female mice, whereas castration of male mice exacerbated psoriasis. Testosterone inhibited both in vitro Th17 differentiation and in vivo IL-17 expression, correlating with reduced psoriasis severity. Molecular studies indicated that testosterone is an inverse agonist of related orphan receptor gamma (RORγt), a key transcription factor for IL-17 expression. These findings offer mechanistic insights into how testosterone limits tissue inflammation in psoriasis and suggest a basis for developing novel testosterone derivatives to target RORγt and suppress Th17-mediated inflammation.</p>\u0000 </div>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neutrophil Heterogeneity Identifies an Association of LAMP1 With Proliferative Lupus Nephritis","authors":"Lennard Ostendorf,&nbsp;Panagiotis Garantziotis,&nbsp;Frank Y. Huang,&nbsp;Georg Schett,&nbsp;Accelerating Medicines Partnership: RA/SLE Network,&nbsp;James A. Lederer,&nbsp;Andrea Fava,&nbsp;Deepak A. Rao,&nbsp;Ricardo Grieshaber-Bouyer","doi":"10.1002/eji.70022","DOIUrl":"https://doi.org/10.1002/eji.70022","url":null,"abstract":"<p>Lupus nephritis (LN) is a severe manifestation of systemic lupus erythematosus (SLE) with limited biomarkers for early detection. While neutrophils contribute to SLE pathogenesis, their phenotypic heterogeneity in disease remains poorly characterized. Here, we used mass cytometry to profile blood neutrophils from patients with biopsy-confirmed proliferative LN and healthy controls. We identified a distinct population of activated neutrophils, marked by surface expression of lysosomal-associated membrane protein 1 (LAMP1/CD107a), that was virtually absent in healthy individuals. We demonstrate that LAMP1 resides intracellularly in resting neutrophils and translocates to the cell surface upon activation. Transcriptomic analysis revealed no difference in LAMP1 mRNA expression between patients with SLE and controls, confirming that surface LAMP1 reflects neutrophil activation rather than increased transcription. Soluble LAMP1 was significantly elevated in serum from patients with SLE compared with controls, with the highest levels in proliferative LN. In a large cohort of 225 patients with LN, urinary LAMP1 correlated with glomerular filtration rate, proteinuria, and histological activity indices. Together, our findings reveal LAMP1 as a marker of neutrophil activation in SLE and identify serum and urinary LAMP1 as potential noninvasive biomarkers for proliferative LN.</p>","PeriodicalId":165,"journal":{"name":"European Journal of Immunology","volume":"55 8","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/eji.70022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144773861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}