Clinical immunology最新文献

{"title":"Autoantibody fine specificity restriction is associated with clinical response in RA treated with abatacept and methotrexate","authors":"Pauline Brevet ,&nbsp;André Gillibert ,&nbsp;Léna Le Goaréguer ,&nbsp;Claire Lattard ,&nbsp;Laurent Drouot ,&nbsp;Rémi Varin ,&nbsp;Marie-Laure Golinski ,&nbsp;Sophie Candon ,&nbsp;Olivier Boyer ,&nbsp;Thierry Lequerré ,&nbsp;Olivier Vittecoq ,&nbsp;Manuel Fréret","doi":"10.1016/j.clim.2025.110610","DOIUrl":"10.1016/j.clim.2025.110610","url":null,"abstract":"<div><h3>Objective</h3><div>Anti-modified protein antibodies (AMPA) are central in rheumatoid arthritis (RA). We evaluated whether changes in fine specificities (FS) of anti-citrullinated protein antibodies (ACPA) and anti-CarP antibodies relate to clinical prognosis in RA patients treated with abatacept (ABA) plus methotrexate (MTX).</div></div><div><h3>Methods</h3><div>A multiplex bead immunoassay measured 6 ACPA FS and 1 anti-CarP FS in 59 anti-CCP+ RA patients (IgG, IgA). Disease activity (DAS28-CRP) and FS levels were assessed at baseline (M0) and 6 months (M6).</div></div><div><h3>Results</h3><div>After 6 months of ABA+MTX, several FS decreased with frequent negative seroconversion (NS). Higher baseline anti-citrullinated α-enolase (ACit-ENO1) IgG levels predicted better outcome (decrease of −0.17 DAS28 score per decile, 95 % CI −0.27 to −0.07, <em>p</em> = 0.03). Among patients with ≥1 positive FS at M0, a higher number of NS across 14 FS (IgG/IgA) correlated with greater improvement (−0.27 DAS28 score per antibody, 95 % CI −0.39 to −0.15, <em>p</em> &lt; 0.0001).</div></div><div><h3>Conclusions</h3><div>In this cohort of limited size, clinical response at M6 with ABA+MTX treatment was associated with the restriction of the autoantibody repertoire of IgG and IgA classes in RA patients.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110610"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145353960","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":"TGF-β: A silent player regulating CD8 T cell memory","authors":"Jesús Daniel Zambrano-Romero ,&nbsp;Diana Berenice Ríos-Ramírez,&nbsp;Verónica Yutsil García-Rasilla,&nbsp;Blanca Estela Ruiz-Medina,&nbsp;Paula Licona-Limón","doi":"10.1016/j.clim.2025.110612","DOIUrl":"10.1016/j.clim.2025.110612","url":null,"abstract":"<div><div>Transforming growth factor β (TGF-β) is recognized as an anti-inflammatory cytokine that negatively affects effector CD8 T cells. However, its impact is not confined to the effector CD8 T cell population; TGF-β also plays a role in suppressing naïve CD8 T cell activation, preserving stemness, and influencing the function and differentiation of memory CD8 T cells. Memory CD8 T cells are vital for eradicating pathogens that have previously infected the host. Both tissue-resident and central memory CD8 T cells have demonstrated a dependency on TGF-β for their differentiation. The mechanisms underlying many of these TGF-β effects remain unclear. This review summarizes the roles of TGF-β in various CD8 T cell subsets, with an emphasis on the memory T cell compartment, and discusses recent findings regarding its influence on memory CD8 T cell differentiation as well as open questions in the field.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110612"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336785","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":"Innate immune response to bacterial infections in hospitalized glucose-6-phosphate dehydrogenase-deficient patients; diagnostic value of white blood cell count","authors":"Islam M. Ghazi ,&nbsp;Ahmed F. Omar ,&nbsp;Wasim S. El Nekidy ,&nbsp;Gehan Harb ,&nbsp;Diaa Alrahmany","doi":"10.1016/j.clim.2025.110613","DOIUrl":"10.1016/j.clim.2025.110613","url":null,"abstract":"<div><h3>Introduction</h3><div>Inherited hematological disorders, affecting immune cell quantity and function, compromise immune system efficiency. Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common X-linked inherited enzymopathy and has been implicated in compromised immune cell function and host defense, and in elevating infection vulnerability. This study explores the impact of G6PD deficiency on immune cellular response and infection-related mortality.</div></div><div><h3>Method</h3><div>Adults with G6PD deficiency and bacterial infections (2017–2021) were analyzed. Demographics, comorbidities, laboratory parameters, and microbiological data were assessed. Cox proportional hazards regression analyzed the association between white blood cell (WBC) count and 28-day mortality. The data analysis was conducted using the R software statistical programming language.</div></div><div><h3>Results</h3><div>The investigation included 334 bacterial infection episodes representing 202 unique patients who fulfilled the inclusion criteria. A 19.2 % 28-day mortality rate was observed. Males, those aged ≥60, and patients with comorbidities had higher mortality. Anemia, high globulin, and elevated liver enzymes were associated with mortality. The majority of patients demonstrated reduced WBC counts (&lt;9.8 × 10⁹/L) during infection, significantly contributing to increased mortality risk (HR: 1.95, <em>p</em> = 0.008). Males exhibited a more pronounced impact. This study reveals heightened mortality risk in G6PD-deficient patients with diminished WBC counts during infections. Elevated CRP, globulins, and liver enzymes indicated severe infections, contrasting the unexpected non-response in WBC counts.</div></div><div><h3>Conclusion</h3><div>Vigilance in treating infections in G6PD-deficient patients, especially in males, is crucial for favorable outcomes. Diagnostic reliance on altered WBC counts in this population may misguide clinical decisions. G6PD deficiency poses a unique challenge in infection management, emphasizing the need for tailored interventions and exploration of alternative biomarkers for assessing severity and predicting mortality. Further studies and larger cohorts are essential for a comprehensive understanding and improved clinical practices.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110613"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318096","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":"The exacerbating role of Ras guanyl-releasing protein 1 in idiopathic inflammatory myopathies","authors":"Marina Kise ,&nbsp;Miku Shimamura ,&nbsp;Natsuka Umezawa ,&nbsp;Nao Tanaka ,&nbsp;Rihan Da ,&nbsp;Shiyao Li ,&nbsp;Tadashi Hosoya ,&nbsp;Tetsuya Saito ,&nbsp;Chikashi Terao ,&nbsp;Shinsuke Yasuda","doi":"10.1016/j.clim.2025.110636","DOIUrl":"10.1016/j.clim.2025.110636","url":null,"abstract":"<div><div>Idiopathic inflammatory myopathies (IIMs) are autoimmune disorders characterized by muscle injury mediated by both T cells and macrophages. Ras guanyl-releasing protein 1 (RasGRP1) is a guanine exchange factor for a small G protein Ras, expressed in immune cells. In this study, we investigated the role of RasGRP1 in IIMs. RasGRP1 was expressed in either CD8+, CD4+ or CD68+ cells in muscles from IIM patients as well as a murine model of myositis, C protein-induced myositis (CIM). RasGRP1 expression was upregulated in activated CD8+ T cells and macrophages <em>in vitro</em>. Response to MHC Class I-restricted stimulation in <em>Rasgrp1−/−</em> CD8+ T cells was impaired. Furthermore, <em>Rasgrp1−/−</em> mice were resistant to CIM. Differentially expressed genes between <em>Rasgrp1−/−</em> and WT mice with CIM were enriched in both adaptive and innate immune responses. These results suggested that RasGRP1 could exacerbate myositis <em>via</em> both T cells and macrophages. RasGRP1 is a possible therapeutic target for IIMs.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110636"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145457768","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":"Immunosenescent and exhausted T cells in systemic lupus erythematosus patients with cognitive impairment","authors":"Erik Cimé-Aké ,&nbsp;Guadalupe Lima ,&nbsp;Emilio Godínez-Lazarini ,&nbsp;Sandra Juárez ,&nbsp;Hilda Marín-López ,&nbsp;Daniela Flores-Hernández ,&nbsp;Ileana Flores-Hernández ,&nbsp;Amairani Gómez-Rodríguez ,&nbsp;Diego F. Hernández-Ramírez ,&nbsp;Luis Llorente ,&nbsp;Hilda Fragoso-Loyo","doi":"10.1016/j.clim.2025.110635","DOIUrl":"10.1016/j.clim.2025.110635","url":null,"abstract":"<div><div>The objective was to assess the expression of senescence and exhaustion markers in CD4⁺ and CD8⁺ T-cell subsets, along with the p16^INK4a gene, in patients with systemic lupus erythematosus (SLE) and cognitive impairment (CI), compared with SLE patients without CI and healthy controls (HC). All participants underwent a standardized neurocognitive test battery, and CI was defined as performance ≥2 SD below the normative mean in ≥1 cognitive domain. The expression of immunosenescence and exhaustion markers was assessed by flow cytometry; expression of p16^INK4a was assessed by qPCR. The SLE-CI group demonstrated a higher CD4⁺/CD8⁺ inverted ratio and increased p16^INK4a expression. Compared with both SLE patients without CI and HC, SLE-CI patients exhibited reduced expression of CTLA-4⁺, LAG-3⁺, and PD-L1⁺ on CD4⁺ T-cells, as well as decreased PD-L1⁺ and TIM-3⁺ expression on CD8⁺ T-cells. Immunosenescence and T-cell exhaustion may contribute to the pathogenesis of CI in SLE.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110635"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145437712","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":"The baseline vaginal immune milieu is an important determinant of the inflammatory response induced by penile-vaginal sex","authors":"Jinny Tsang ,&nbsp;Avid Mohammadi ,&nbsp;Sareh Bagherichimeh ,&nbsp;Yoojin Choi ,&nbsp;Azadeh Fazel ,&nbsp;Elizabeth Tevlin ,&nbsp;Sanja Huibner ,&nbsp;Sara V. Good ,&nbsp;Wangari Tharao ,&nbsp;Bryan Coburn ,&nbsp;Rupert Kaul","doi":"10.1016/j.clim.2025.110615","DOIUrl":"10.1016/j.clim.2025.110615","url":null,"abstract":"<div><div>Elevated cervicovaginal cytokines/chemokines and epithelial disruption are associated with HIV risk. While penile-vaginal sex induces transient cervicovaginal inflammation and epithelial disruption, there is considerable interindividual heterogeneity. We defined genital inflammation using a multi-cytokine score and hypothesized that sex-induced inflammation would depend on the pre-existing vaginal immune milieu. We quantified HIV-associated immune factors in cervicovaginal secretions of HIV-uninfected women before and 1 h after penile-vaginal sex. Cervicovaginal IgA and IgG increased after sex, and baseline IgA was associated with inflammatory cytokines and epithelial disruption. Post-sex vaginal immune factors strongly associated and clustered with pre-sex concentrations, and participants with baseline inflammation remained inflamed after sex. Sex induced greater relative changes in inflammatory cytokines and epithelial disruption among participants with lower baseline levels, but not in chemokines. In conclusion, the baseline vaginal milieu determines the inflammatory effects of sex; specifically, sex elicits a greater change in inflammatory responses in women with baseline vaginal immunoquiescence.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110615"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145463283","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":"Leukemia inhibitory factor (LIF) in acute graft-versus-host disease: A hypothesis-generating review","authors":"Ahmad Meshkin ,&nbsp;Fateme Zare ,&nbsp;Mohammad Erfan Abbasi ,&nbsp;Maryam sadat Montazeri ,&nbsp;Fatemeh Badiee ,&nbsp;Mohammad Masoud Khodaei","doi":"10.1016/j.clim.2025.110640","DOIUrl":"10.1016/j.clim.2025.110640","url":null,"abstract":"<div><div>Leukemia inhibitory factor (LIF) is a multifunctional cytokine of the IL-6 family, originally identified in murine leukemia cells. Graft-versus-host disease (GvHD) is a major complication of allogeneic hematopoietic stem cell transplantation (allo-HSCT), primarily affecting the intestine, liver, and skin. Preclinical studies suggest that LIF may protect against GvHD by preserving intestinal stem cells, reducing radiation- and cytokine-induced tissue injury, decreasing donor T-cell infiltration, and suppressing inflammatory cytokine production; importantly, it appears to preserve graft-versus-leukemia (GVL) activity. This review summarizes current knowledge on the immunopathogenesis of acute GvHD (aGvHD) and examines the emerging but limited evidence on the immunomodulatory role of LIF. We propose a hypothesis-driven framework for its potential therapeutic application. We highlight the immunomodulatory properties of LIF, including its roles in suppressing proinflammatory responses and promoting regulatory mechanisms. LIF's ability to reduce GvHD severity without compromising GVL highlights its potential as a therapeutic agent. Given the limited but promising data, further research is warranted to evaluate LIF's clinical applicability and safety in transplant recipients.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"282 ","pages":"Article 110640"},"PeriodicalIF":3.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530317","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":"ILT-2 and ILT-4 expression and donor genotype as factors associated with HSCT outcome","authors":"Jagoda Siemaszko ,&nbsp;Piotr Łacina ,&nbsp;Donata Szymczak ,&nbsp;Agnieszka Szeremet ,&nbsp;Maciej Majcherek ,&nbsp;Anna Czyż ,&nbsp;Małgorzata Sobczyk-Kruszelnicka ,&nbsp;Wojciech Fidyk ,&nbsp;Iwona Solarska ,&nbsp;Barbara Nasiłowska-Adamska ,&nbsp;Patrycja Skowrońska ,&nbsp;Maria Bieniaszewska ,&nbsp;Agnieszka Tomaszewska ,&nbsp;Grzegorz W. Basak ,&nbsp;Sebastian Giebel ,&nbsp;Tomasz Wróbel ,&nbsp;Katarzyna Bogunia-Kubik","doi":"10.1016/j.clim.2025.110605","DOIUrl":"10.1016/j.clim.2025.110605","url":null,"abstract":"<div><h3>Background</h3><div>NK cell activity after allogeneic haematopoietic stem cell transplantation (HSCT) is still not fully understood. Their cytotoxic activity is modulated by a range of inhibitory and activating surface receptors. Among these, the inhibitory receptors ILT-2 and ILT-4 have yet to be explored in relation to HSCT and its outcomes.</div></div><div><h3>Methods</h3><div>Genotyping for ILT-2 and ILT-4 was performed using TaqMan assays. ILT-2 and ILT-4 surface expression on NK cells was assessed by flow cytometry. Levels of sHLA-F and sHLA-G were determined using ELISA. mRNA expression of <em>ILT-2</em>, <em>ILT-4</em> and <em>IFN-γ</em> was measured with quantitative real-time PCR with TaqMan Gene Expression probes.</div></div><div><h3>Results</h3><div>Presence of donor ILT-2 rs1061681 <em>T</em> allele was associated with increased risk of chronic graft-versus-host disease (cGVHD) (<em>p</em> = 0.0239). Donor ILT-4 rs1128646 <em>T</em> allele was related with decreased risk of overall survival after HSCT (<em>p</em> = 0.0506) and with higher risk of acute GvHD (aGvHD) (<em>p</em> = 0.0834). Serum levels of sHLA-F and sHLA-G were significantly higher at day +30 than day +90 after HSCT (<em>p</em> = 0.0002 and <em>p</em> &lt; 0.0001, respectively). Expression of ILT2 at mRNA level was significantly decreased among recipients with aGvHD (<em>p</em> = 0.0266). ILT-4 expression correlated negatively with expression of interferon gamma (<em>p</em> = 0.0280, R = -0.532). The percentages of <em>LILRB1</em>/ILT-2+ and <em>LILRB2</em>/ILT4+ NK cells were the highest at day +21 after HSCT (<em>p</em> = 0.0014 and <em>p</em> &lt; 0.0001 for ILT-2 and ILT-4, respectively).</div></div><div><h3>Conclusions</h3><div>Both ILT-2 and ILT-4 inhibitory receptors were found to be associated with allogeneic HSCT outcome. This suggests that ILT receptor expression on NK cells may potentially play a role in post-transplant complications.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110605"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228466","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":"Ferroptosis in patients with rheumatoid arthritis","authors":"Yunping Cai ,&nbsp;Jingjing Dou ,&nbsp;Nihong Zhou ,&nbsp;Han Shao ,&nbsp;Xian Shen ,&nbsp;Cui Lu ,&nbsp;Xiaoli Fan ,&nbsp;Song Guo Zheng","doi":"10.1016/j.clim.2025.110588","DOIUrl":"10.1016/j.clim.2025.110588","url":null,"abstract":"<div><h3>Background</h3><div>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently emerged as a potential contributor to RA pathogenesis.</div></div><div><h3>Methods</h3><div>A systematic literature review was conducted to explore the mechanisms of ferroptosis in RA, focusing on iron metabolism dysregulation, oxidative stress, and immune cell dysfunction. Databases including PubMed, Embase, and Web of Science were searched for relevant studies.</div></div><div><h3>Results</h3><div>RA patients exhibit paradoxical iron distribution, with systemic deficiency but synovial overload, promoting ferroptosis. Key findings include: (1) Iron accumulation and lipid peroxidation exacerbate synovial inflammation; (2) Ferroptosis differentially affects immune cells (M1/M2 macrophages, T cells) and fibroblast-like synoviocytes (FLS); (3) Antioxidant defenses (GPX4) are impaired in RA, while some disease-modifying drugs (leflunomide, sulfasalazine) may modulate ferroptosis.</div></div><div><h3>Conclusion</h3><div>Ferroptosis plays a critical role in RA progression by disrupting synovial homeostasis. Targeting ferroptosis pathways offers promising therapeutic potential, though further research is needed to clarify cell-specific effects and optimize interventions.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110588"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144921605","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":"CD14+CD11c+HLA-II− monocytes are identified to be associated with osteoclastogenesis in ankylosing spondylitis","authors":"Lian Gui ,&nbsp;Zena Chen ,&nbsp;Liudan Tu ,&nbsp;Liuzhong Zhou ,&nbsp;Qiujing Wei ,&nbsp;Jieruo Gu","doi":"10.1016/j.clim.2025.110586","DOIUrl":"10.1016/j.clim.2025.110586","url":null,"abstract":"<div><div>Abnormal monocytes are involved in the pathogenesis of ankylosing spondylitis (AS). We investigated the association between an imbalance of monocyte subpopulations and bone destruction in AS. Compared to controls, AS patients exhibited increased CD14⁺CD11c⁺HLA-II⁻ monocytes and decreased CD14⁺CD11c⁺HLA-II⁺ monocytes in peripheral blood. LPS stimulation promoted a shift from CD14⁺CD11c⁺HLA-II⁻ monocytes toward CD14⁺CD11c⁺HLA-II⁺ monocytes, enhancing the former's capacity to promote CD4⁺ T cell proliferation. Micro RNA-seq analysis indicated that AS CD14⁺CD11c⁺HLA-II⁻ monocytes were involved in osteoclast differentiation and overproduced soluble osteoclastogenic cytokine CSF-1. In 40 AS patients, evaluated CD14⁺CD11c⁺HLA-II⁻ monocytes correlated positively with Spondyloarthritis Research Consortium of Canada (SPARCC) MRI inflammation score (<em>r</em> = 0.336, <em>P</em> = 0.034) and bone erosion score (<em>r</em> = 0.423, <em>P</em> = 0.007), but inversely with ankylosis score (<em>r</em> = −0.346, <em>P</em> = 0.029). Conversely, CD14⁺CD11c⁺HLA-II⁺ monocytes showed the opposite correlation. Our findings demonstrate that expansion of CD14⁺CD11c⁺HLA-II⁻ monocytes contribute to bone erosion in AS, potentially mediated through CSF-1-driven osteoclast differentiation.</div></div>","PeriodicalId":10392,"journal":{"name":"Clinical immunology","volume":"281 ","pages":"Article 110586"},"PeriodicalIF":3.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144879551","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}