Immunology letters最新文献

{"title":"Sepsis as a complex syndrome: Are combined biomarkers the future of diagnosis and prognosis? Clinical perspective","authors":"R. Gaderparnah ,&nbsp;F. van Beuningen ,&nbsp;Y. Lin ,&nbsp;S.H. Sadrian ,&nbsp;H.M. Reijneveld ,&nbsp;H. Krabbe ,&nbsp;P. Jonkheijm ,&nbsp;H.R. Bouma ,&nbsp;R.T. Mankowski","doi":"10.1016/j.imlet.2025.107072","DOIUrl":"10.1016/j.imlet.2025.107072","url":null,"abstract":"<div><div>Sepsis remains a major cause of mortality worldwide, driven by a dysregulated host response to infection that leads to life-threatening organ dysfunction. Despite advances in evidence-based medicine, early diagnosis and risk stratification remain significant challenges due to the complex, multifaceted nature of sepsis and substantial interindividual variability in clinical presentation. Current approaches relying on single biomarkers cannot provide comprehensive insights into disease progression, limiting their clinical utility in guiding timely and effective interventions. Given the limitations of current single biomarkers in capturing the complexity of sepsis, there is an urgent need for improved diagnostic approaches. While the discovery of novel biomarkers remains important, combining existing biomarkers may offer a pragmatic and effective strategy to improve diagnostic accuracy by leveraging the strengths of each to compensate for the limitations of other. In this clinical perspective, we highlight the potential of such combined biomarker strategies to enhance diagnostic accuracy, support identification of the infection source, and improve prognostic assessment across the clinical course and into long-term outcomes. We provide examples of key biomarkers and their synergistic potential, emphasizing the need for advanced analytical methods such as machine learning and multi-omics integration to enhance predictive accuracy. Shifting toward multi-component biomarker panels represents a critical step toward a more precise, personalized approach to sepsis management to reduce sepsis-related morbidity and mortality. We advocate for further research and validation efforts to facilitate the clinical implementation of combined biomarker models, ultimately transforming sepsis care.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107072"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144890650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD4 and CD8 T-cell lymphocytes from penile squamous cell carcinoma tumors are more differentiated with higher PD-1 expression compared to lymphocytes in peripheral circulation","authors":"Chibamba Mumba ,&nbsp;Nicholas K. Mwale ,&nbsp;Victor Mapulanga ,&nbsp;Owen Ngalamika","doi":"10.1016/j.imlet.2025.107099","DOIUrl":"10.1016/j.imlet.2025.107099","url":null,"abstract":"<div><h3>Background</h3><div>Penile squamous cell carcinoma (PSCC) is the commonest malignancy of the penis, with a higher incidence and poor treatment outcomes in developing countries. T-cell phenotypes have been shown to identify patients who may respond favorably to immune therapy, and also associate with treatment outcomes. This study aimed to determine and compare the tumor and peripheral blood T-cell phenotypes of individuals with PSCC, and whether factors such as smoking and presence of HPV associate with these T-cell phenotypes.</div></div><div><h3>Methods</h3><div>We conducted a prospective cross-sectional study at the University Teaching Hospital, Lusaka, Zambia. Participants with a histologically-confirmed PSCC were recruited into the study. Socio-demographic information was obtained, and whole blood was collected and subjected to peripheral blood mononuclear cells (PBMCs) isolation. Fresh penile tumors were mechanically and enzymatically digested. CD4 and CD8 cells were sorted from PBMCs and tumor, stained using antibodies against CD3, CD45RO, CCR7, PD-1, CD103 and CD69, and subjected to flow cytometry. Parts of the tumor were subjected to HPV detection, and histological grading and staging.</div></div><div><h3>Results</h3><div>Twenty-four participants were recruited into the study. The median age was 55.5 years, 45.8 % were smokers, 87.5 % were HIV positive, 62.5 % had high-risk HPV detected in the tumors, and 25 % had advanced-stage disease. There was a significantly higher proportion of naïve cells among CD4 T-cells from PBMCs than tumor (40.2 % vs 3.8 %; p = 0.01). CD4 T cells from the tumor demonstrated a significantly higher proportion of cells expressing CD69 (3.2 % vs 95.9 %; p = 0.0001), CD103 (0.7 % vs 7.3 %; p = 0.0001), and PD-1 (35.5 % vs 92 %; p = 0.0001) than the ones from PBMCs. Tumoral CD8 T-cells had a significantly lower proportion of terminally-differentiated effector cells but higher proportion of central memory cells compared to PBMCs, (7.9 % vs 15.1 %, p = 0.04) and (55 % vs 14.4 %; p = 0.01) respectively. Tumoral CD8 T-cells also had a significantly higher proportion of cells expressing CD69 (96.7 % vs 8.5 %; p = 0.0001), CD103 (22.2 % vs 1.2 %; p = 0.0001), and PD-1 (79.3 % vs 18.8 %; p = 0.0001) when compared to the PBMCs. Early-stage disease was associated with a significantly higher proportion of central memory CD4 T-cells among the PBMCs when compared with advanced stage disease (46.7 % vs 30 %; p = 0.01), while smoking was associated with a significantly higher proportion of tumoral CD8 T-cells expressing the homing marker CD103 (28.2 % vs 17.8 %; p = 0.01).</div></div><div><h3>Conclusion</h3><div>PSCC tumors demonstrate a higher proportion of primed T-cells with a memory phenotype compared to T-cells in the circulation. T-cells from PSCC tumors also have a higher proportion of cells expressing the immune checkpoint PD-1 and homing markers than those from the circulation.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"277 ","pages":"Article 107099"},"PeriodicalIF":2.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the biological potential of skin fibroblast: responses to TNF-α, highlighting intracellular signaling pathways and secretome","authors":"Carlota Pascoal ,&nbsp;Pedro Granjo ,&nbsp;Patrícia Mexia ,&nbsp;Diana Gallego ,&nbsp;Rita Adubeiro Lourenço ,&nbsp;Shally Sharma ,&nbsp;Bélen Pérez ,&nbsp;Margarida Castro-Caldas ,&nbsp;Ana Rita Grosso ,&nbsp;Vanessa dos Reis Ferreira ,&nbsp;Paula Alexandra Videira","doi":"10.1016/j.imlet.2025.107057","DOIUrl":"10.1016/j.imlet.2025.107057","url":null,"abstract":"<div><h3>Objective</h3><div>In this study, we examined the molecular response of human skin fibroblasts to an inflammatory cytokine to evaluate their suitability as models for immunopathology research.</div></div><div><h3>Methods</h3><div>Skin fibroblasts were stimulated with tumour necrosis factor (TNF)-α, and the transcriptome was profiled via RNA-Seq. The differentially expressed genes were screened to predict immunological pathways and interactions. The cytokines and signaling pathways were validated at protein level. Similarly to immune cells, TNF-α caused transcriptional and transductional changes in fibroblasts.</div></div><div><h3>Results</h3><div>Functional analysis revealed significant enrichment of TNF-α signaling and cell chemotaxis (normalized enrichment score = 2.59 and 3.42). We also detected enrichment of nuclear factor kappa B (NF-κB) target genes and NF-kB activation, confirmed by complete protein degradation of its inhibitor IκBa (<em>p</em> = 0.0019). The MAPK/ERK and p38 MAPK pathways were also activated. Finally, we observed significant secretion of proinflammatory cytokines and chemokines, such as interleukin 6 (<em>p</em> = 0.02), CXCL8 (<em>p</em> = 0.027), CCL2 (<em>p</em> = 0.028) and CCL5 (<em>p</em> = 0.016).</div></div><div><h3>Conclusion</h3><div>This study advances the biological understanding of skin fibroblast responses to TNF-α, revealing their intracellular pathways and secretome. It discloses techniques for leveraging fibroblasts' potential as <em>in vitro</em> models to identify inflammatory drivers, particularly when alternative models are inaccessible.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107057"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144575402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Schizophrenia-associated complement component C4 induces maturation and reactivity in human astrocytes","authors":"Isabella de Sousa Nóbrega,&nbsp;Melissa Bernardini Bachir Moysés,&nbsp;Bruno Yukio Yokota-Moreno,&nbsp;Guilherme Grecco Ferreira,&nbsp;Guilherme Martelossi Cebinelli,&nbsp;Andréa Laurato Sertié","doi":"10.1016/j.imlet.2025.107065","DOIUrl":"10.1016/j.imlet.2025.107065","url":null,"abstract":"<div><div>Beyond its canonical role in innate immunity, the complement system (CS) has been increasingly implicated in brain development and disease. Elevated expression of complement component C4, in particular, is strongly associated with an increased risk of schizophrenia (SCZ), potentially by promoting excessive synaptic pruning. Astrocytes, the primary producers of CS components in the brain and expressers of multiple CS receptors, play crucial roles in synaptic formation and refinement. Dysregulated C4 levels may therefore impair astrocyte function, disrupt synaptic development, and contribute to SCZ pathogenesis. In this study, we investigated the direct effects of exogenous C4 on astrocyte differentiation, maturation, and reactivity using human induced pluripotent stem cell (hiPSC)-derived astrocytes. Astrocytes were treated with recombinant human C4 protein either chronically during differentiation or acutely after maturation. While chronic C4 exposure did not significantly affect astrocyte differentiation, both treatment regimens induced phenotypic features of astrocyte maturation and reactivity. These included upregulation of reactive astrocyte markers (CD44 and GFAP), morphological changes consistent with mature and reactive states, and nuclear translocation of NF-κB. Mechanistically, these effects may be mediated, at least in part, by activation of the MAPK/ERK pathway and suppression of mTORC1 signaling. Together, our findings suggest that elevated C4 levels promote astrocyte maturation and reactivity, providing new insights into the mechanisms by which complement dysregulation may contribute to SCZ pathogenesis.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107065"},"PeriodicalIF":2.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144768614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Antibodies to expanded virus antigen panels show elevated diagnostic sensitivities in multiple sclerosis and optic neuritis” [Immunol. Lett. 254 (2023) 54–64]","authors":"Helena Gåsland ,&nbsp;Nicole H Trier ,&nbsp;Cecilie Kyllesbech ,&nbsp;Anette H Draborg ,&nbsp;Rimantas Slibinskas ,&nbsp;Evaldas Ciplys ,&nbsp;Danguolė Žiogienė ,&nbsp;Alma Gedvilaitė ,&nbsp;Rasa Petraitytė-Burneikienė ,&nbsp;Jette L Frederiksen ,&nbsp;Gunnar Houen","doi":"10.1016/j.imlet.2025.107067","DOIUrl":"10.1016/j.imlet.2025.107067","url":null,"abstract":"","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107067"},"PeriodicalIF":2.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144845782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynactin subunit 1 facilitates mast cell degranulation to drive food allergy pathogenesis","authors":"Miao Zhao ,&nbsp;Hanqing Zhang ,&nbsp;Zhiqiang Liu ,&nbsp;Jiangqi Liu ,&nbsp;Bailing Xie ,&nbsp;Lu Zeng ,&nbsp;Xiangyu Wang ,&nbsp;Qing Shu ,&nbsp;Ping Tang ,&nbsp;Lihua Mo ,&nbsp;Haotao Zeng ,&nbsp;Pingchang Yang","doi":"10.1016/j.imlet.2025.107035","DOIUrl":"10.1016/j.imlet.2025.107035","url":null,"abstract":"<div><h3>Background</h3><div>Mast cells play pivotal roles in allergic pathogenesis and inflammatory disorders, with their pathologic effects largely mediated through granule exocytosis. Dynactin subunit 1 (Dctn1), a microtubule-associated motor protein, remains unexplored in mast cell-driven inflammation. This study investigates Dctn1’s functional role in regulating mast cell degranulation during food allergy (FA).</div></div><div><h3>Methods</h3><div>An ovalbumin-sensitized murine FA model was established to profile mast cell activity. Gut lavage fluid (GLF) was analyzed via Olink proteomics and ELISA to quantify Dctn1 levels and mast cell mediators (histamine, Mcpt1). Mechanistic studies employed RNA interference, conditional knockout mice (<em>Dctn1</em>^f/f <em>Cma1</em>-Cre), and immunoprecipitation to assess Dctn1’s role in granule trafficking.</div></div><div><h3>Results</h3><div>FA mice exhibited 3.2-fold higher Dctn1 levels in GLF versus controls (<em>p</em> &lt; 0.001), strongly correlating with mast cell mediator concentrations (histamine: <em>r</em> = 0.73; Mcpt1: <em>r</em> = 0.7). Intestinal mast cells showed selective Dctn1 upregulation (2.8-fold mRNA increase, <em>p</em> &lt; 0.01), mechanistically linked to granule trafficking through CMA1 complex formation. Mast cell-specific Dctn1 ablation reduced Mcpt1 release by 74 % (<em>p</em> &lt; 0.001) and ameliorated FA symptoms (92 % core temperature drop, <em>p</em> &lt; 0.005), independent of AKT/ERK signaling pathways.</div></div><div><h3>Conclusions</h3><div>This study identifies Dctn1 as a novel regulator of mast cell degranulation in FA, operating through microtubule-dependent granule transport. Targeted inhibition of Dctn1 significantly attenuates allergic responses without disrupting canonical activation signals, positioning it as a promising therapeutic target for mast cell-driven pathologies.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107035"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-125a-5p regulates Treg function by targeting Foxp3 in experimental autoimmune myasthenia gravis mice","authors":"Shuting Tan,&nbsp;Jingli Liu,&nbsp;Liuling Chen,&nbsp;Ruying Li,&nbsp;Jinpin Li","doi":"10.1016/j.imlet.2025.107050","DOIUrl":"10.1016/j.imlet.2025.107050","url":null,"abstract":"<div><div>MicroRNAs are a class of endogenous noncoding small RNAs. miR-125a-5p is involved in immunoregulatory mechanisms in autoimmune diseases. Myasthenia gravis (MG) is an autoimmune disease in which regulatory T cells (Tregs) exhibit reduced numbers and functional defects, with decreased expression of the Treg cell-specific transcription factor Foxp3. Our previous study identified an abnormally high expression of miR-125a-5p in thymoma-associated myasthenia gravis, however, the involvement of miR-125a-5p in the pathogenesis of myasthenia gravis in vivo is unclear. In this study, we explored the role of thymic miR-125a-5p abnormalities in the pathogenesis of myasthenia gravis by establishing an experimental autoimmune myasthenia gravis model. Muscle strength score, low-frequency repetitive nerve stimulation, and serum acetylcholine receptor antibody were performed. The relative expression of miR-125a-5p and Foxp3 in the thymus and spleen was quantified, and the percentage of Treg cells, the levels of the inhibitory cytokines IL-10 and TGF-β1, and the proliferative capacity of splenic T lymphocytes were detected. Our findings revealed significant upregulation of miR-125a-5p expression in myasthenia gravis models. Reducing miR-125a-5p levels alleviated muscle weakness symptoms, elevated Foxp3 expression, enhanced the number of Treg cells, elevated the levels of the Treg-associated inhibitory cytokines IL-10 and TGF-β1, and inhibited the proliferative function of splenic T lymphocytes. The opposite result was obtained when miR-125a-5p was overexpressed. These results suggest that miR-125a-5p can inhibit Foxp3 expression, leading to a decrease in the number and abnormal function of Treg cells. Thus, our findings suggest that miR-125a-5p participates in the pathogenesis of myasthenia gravis by targeting Foxp3 to regulate the function of Treg cells, providing new insights to explore the immunoregulatory mechanisms of miR-125a-5p in myasthenia gravis.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107050"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B cells are major players in cancer immunity","authors":"Théo Bouloudani ,&nbsp;Guilhem Pupier ,&nbsp;Catherine Sautès-Fridman ,&nbsp;Wolf Herman Fridman","doi":"10.1016/j.imlet.2025.107064","DOIUrl":"10.1016/j.imlet.2025.107064","url":null,"abstract":"<div><div>The discovery of Tertiary Lymphoid Structures (TLS) within tumors has reshaped our understanding of cancer immunity. Unlike the classical view that immune responses are solely initiated in lymph nodes, TLS, ectopic lymphoid aggregates resembling secondary lymphoid organs, can form in the tumor microenvironment (TME). These structures contain T cells, B cells, dendritic cells (DC) presenting antigenic peptides to T cells in the T cell zone of TLS, and follicular dendritic cells (FDC) which are stromal cells involved in the formation of germinal centers (GCs) and presenting antigens, under the form of immune complexes, to B cells. Mature TLS with GCs support B cell differentiation into antibody-producing plasma cells (PCs). Clinical studies reveal that TLS presence correlates with improved survival and response to immunotherapy across multiple cancers, including melanoma, NSCLC, and renal cell carcinoma. Notably, B cells within TLS undergo clonal expansion, somatic hypermutation, and isotype switching, generating tumor-reactive antibodies (IgG, IgA). IgG-opsonized tumor cells can be eliminated by macrophages or NK cells via antibody-dependent cell mediated cytotoxicity or apoptosis by macrophages via antibody-dependent phagocytosis whereas IgA may have dual roles, sometimes promoting immunosuppression. Additionally, B cells enhance antigen presentation to T cells, amplifying anti-tumor responses. Emerging strategies aim to induce TLS formation (e.g., via CXCL13, lymphotoxins…) or harness B cells for adoptive therapies. Future research should clarify tumor-specific antibody targets and optimize TLS induction to enhance immunotherapy.</div><div>In summary, TLS and B cells are pivotal in shaping anti-tumor immunity, offering novel biomarkers and therapeutic avenues for cancer treatment.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107064"},"PeriodicalIF":2.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144764884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic syndrome and inborn errors of immunity: A plausible connection","authors":"Mohit,&nbsp;Sheetal Verma,&nbsp;Vijay Laxmi,&nbsp;Jayhind Maury","doi":"10.1016/j.imlet.2025.107068","DOIUrl":"10.1016/j.imlet.2025.107068","url":null,"abstract":"<div><div>Inborn errors of immunity (IEI), traditionally known as primary immunodeficiencies, are genetically driven disorders that impair immune function. Emerging evidence suggests a strong connection between IEI and metabolic syndrome, including obesity, insulin resistance, and cardiovascular diseases, highlighting the complex interplay between immune and metabolic pathways. This review focuses on how changes in key immune regulatory genes can lead to both immune dysfunction and metabolic problems. Genome Wide Association Studies (GWAS) and Next Generation Sequencing (NGS) have identified numerous genetic variants that link immune and metabolic dysregulation. Both immune system dysfunction and metabolic imbalances are associated with mutations in several key genes such as STAT3, NLRP3, and FOXP3. Pharmacological interventions targeting inflammatory pathways, such as cytokine inhibitors and inflammasome modulators, offer promising therapeutic strategies to address both aspects of these intertwined conditions. Moreover, lifestyle modifications, including anti-inflammatory diets and physical activity, are essential components of a comprehensive approach to mitigate inflammation and improve metabolic outcomes. Advances in genomic profiling drive precision medicine, enabling the tailoring of treatments based on individual genetic variants, optimizing therapy for both immune and metabolic dysfunction. Personalized risk assessments incorporating genetic data further refine preventive strategies for metabolic syndrome. This cited approach underscores the importance of a holistic, integrated approach to unraveling the shared mechanisms of immune and metabolic dysregulation, offering insights into novel diagnostic and therapeutic strategies for these multifactorial disorders.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107068"},"PeriodicalIF":2.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reactive oxygen species production by monocytes negatively correlates with disease activity in rheumatoid arthritis","authors":"Pablo Lores ,&nbsp;Monique Costa ,&nbsp;Anderson Saravia ,&nbsp;Mercedes Landeira ,&nbsp;Valeria da Costa ,&nbsp;Santiago A. Rodríguez-Zraquia ,&nbsp;M. Eugenia Cedrés ,&nbsp;Juan Oliva ,&nbsp;Guillermina Rado ,&nbsp;Ignacio García ,&nbsp;M. Florencia Festari ,&nbsp;Sandra Consani ,&nbsp;Carolina Díaz ,&nbsp;Teresa Freire","doi":"10.1016/j.imlet.2025.107052","DOIUrl":"10.1016/j.imlet.2025.107052","url":null,"abstract":"<div><div>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by severe joint inflammation, synovial hyperplasia and degradation of the cartilage and bone in the joint. Patients with RA have an amplified T helper (Th) 1 and Th17 immune response and production of autoantibodies by autoreactive B cells. In the joint, macrophages mediate bone destruction and maintain the inflammatory process in RA. There is an increasing body of evidence indicating that NADPH oxidase (NOX2)-derived reactive oxygen species (ROS), mainly produced by macrophages and neutrophils, may have effector functions in RA.</div><div>In this work we characterized ROS production in both monocytes and macrophages in RA. Our results indicate that NOX2-dependent production of ROS attenuates inflammation and clinical signs by decreasing innate and adaptive immune responses in collagen-induced arthritis in mice. We also report that ROS production by circulating classical and non-classical monocytes from patients with RA negatively correlate with disease symptoms. Therefore, ROS produced by different monocyte subsets in peripheral blood might be considered as useful biomarkers or predictors of the immune response associated with RA disease activity.</div></div>","PeriodicalId":13413,"journal":{"name":"Immunology letters","volume":"276 ","pages":"Article 107052"},"PeriodicalIF":3.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}