Journal of Leukocyte Biology最新文献

{"title":"Streptococcus anginosus Activates the NLRP3 Inflammasome to Promote Inflammatory Responses from Macrophages.","authors":"Anika M Arias, Dakota M Reinartz, Chloe Sairs, Sangeetha Senthil Kumar, Harrison C Byrnes, Justin E Wilson","doi":"10.1093/jleuko/qiag061","DOIUrl":"https://doi.org/10.1093/jleuko/qiag061","url":null,"abstract":"<p><p>Chronic inflammation and oral dysbiosis are common features of oral squamous cell carcinoma (OSCC). The commensal streptococci, S. anginosus, is increased in oral diseases including OSCC. Our previous work revealed that S. anginosus promotes inflammatory responses from macrophage cell lines, however the molecular mechanism by which S. anginosus interacts with macrophages to instigate this response remains to be investigated. Here, we found S. anginosus activated primary bone marrow derived macrophages (BMMs), which presented increased NF-κB activation and downstream inflammatory cytokines TNF⍺, IL-6 and IL-1β at 24 hours post-infection. S. anginosus viability, TLR2, TLR4 and MyD88 were dispensable for NF-κB activation, but each promoted the induction of distinct downstream inflammatory mediators, with only MyD88 being necessary for NF-κB activation in response to heat-killed S. anginosus. S. anginosus replicated intracellularly within BMMs without causing cell death and induced expression of inflammasome sensors AIM2, NLRC4 and NLRP3. S. anginosus-infected BMMs lacking the inflammasome adapter protein ASC (Asc-/-) or Caspase-1 (Caspase1-/-) had significantly diminished IL-1β production compared to wild type BMMs, indicating that S. anginosus activated the inflammasome. S. anginosus primarily triggered the inflammasome through NLRP3 as S. anginosus-infected Nlrp3-/- BMMs and NLRP3 inhibitor (MCC950)-treated wild type BMMs displayed diminished IL-1β production compared to wild type controls. Lastly, S. anginosus-infected Asc-/- and to a lesser extent Nlrp3-/- mice displayed reduced weight loss, reduced inflammatory cytokines, and increased bacterial burden compared to C57BL/6 mice. These findings indicate that S. anginosus replicates within macrophages and promotes a proinflammatory response in part through activating the NLRP3 inflammasome.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839043","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":"Chemokine receptor expression defines a trajectory from monocytes to mature macrophages in the lung.","authors":"Heather Mathie, Laura Medina-Ruiz, Fabian Schuette, Heba Halawa, Zuzanna Pocalun, Elise Pitmon, John Cole, Marieke Pingen, Gerard J Graham","doi":"10.1093/jleuko/qiag059","DOIUrl":"https://doi.org/10.1093/jleuko/qiag059","url":null,"abstract":"<p><p>CCR1, CCR2 and CCR5 direct recruitment of monocytes and macrophages in inflammation. However, the discrete role for each receptor in monocyte/macrophage biology remains poorly understood, with previous reports citing receptor redundancy. Using transcriptomic approaches to examine inflammatory chemokine receptor expression on lung interstitial macrophage populations, we demonstrate that interstitial macrophages can be divided into three distinct subsets, each of which express specific patterns of chemokine receptors, and that there are dynamic changes in chemokine receptor expression as macrophages differentiate from monocytes in the lung. Furthermore, macrophages expressing different combinations of chemokine receptors are transcriptionally distinct, suggesting non-redundant functions for CCR1, 2 and 5. Finally, we examined changes in macrophage chemokine receptor expression in vitro after treatment with varied TLR ligands, and show that CCR1 is specifically increased in response to bacterial but not viral ligands. Our data provide compelling evidence that macrophage chemokine receptor expression is not redundant, but specific and malleable in response to discrete inflammatory stimuli.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838964","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":"Immune Landscape of COVID-19 recovery: Nucleocapsid as a major target of CD8+ T cell antiviral responses in convalescent HLA-A*2+ individuals from Brazil.","authors":"Ágata Lopes-Ribeiro, Geovane Marques-Ferreira, Franklin Pereira Araujo, Patrícia de Melo Oliveira, Alice Aparecida Lourenço, Laura Cardoso Corrêa-Dias, Thaíza Aline Pereira Santos, Caio Wilker Teixeira, Letícia Gomes de Pontes, Victor de Melo Rocha, Erik Vinicius de Sousa Reis, Samille Henriques Pereira, Adriana Alves Oliveira Paim, Luis Adan Flores Andrade, Camila Pacheco Silveira Martins da Mata, Flávio Guimarães da Fonseca, Fernanda Daniela Santos Coelho, Rafael Pacheco Coelho, Gabriel Pacheco Coelho, Vanessa Peruhype-Magalhães, Andréa Teixeira-Carvalho, Olindo Assis Martins-Filho, Afshin Beheshti, Moriya Tsuji, Jordana Grazziela Alves Coelho-Dos-Reis","doi":"10.1093/jleuko/qiag050","DOIUrl":"https://doi.org/10.1093/jleuko/qiag050","url":null,"abstract":"<p><p>Despite advanced knowledge on the SARS-CoV-2-induced immunity, a deeper understanding of how virus-specific responses are assembled upon infection is necessary. Therefore, the present work investigates the MHC-restricted virus-specific responses of acute and post-acute COVID-19 patients. Our results indicate that convalescent individuals displayed and maintained higher counts of effector memory, and TEMRA CD4+ T and CD8+ T cells as compared to severe COVID-19. Mild COVID-19 displayed a higher early activation profile in memory subsets as compared to severe and convalescent individuals. Regarding the virus-specific T cell responses, SARS-CoV-2 nucleocapsid protein (N) arose as a major target of CD8+ T cells in convalescent HLA-A*2+ individuals, adding to the specific cellular response mediated by the spike (S) protein. Unsupervised analysis enabled the unbiased clustering of lymphocytes and the assessment of differential expression of CD69, production of intracellular IFN-γ, and reactivity to HLA-A*02 tetramers bearing N or S peptides. Furthermore, cell clones targeting S and N proteins of SARS-CoV-2 undergo cellular expansion in HLA-A*02+ convalescent individuals following in vitro antigenic recall by stimulation with inactivated SARS-CoV-2 and viral proteins. Convalescent from COVID-19 presents higher connectivity of the overall immune response in comparison to the acute phase, regardless of disease severity. Collectively, our data shed new light on the role of the protein N-mediated immunity against SARS-CoV-2 in patients from one of the most affected areas in Brazil.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839016","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":"BET inhibition curbs macrophage inflammation, lipid accumulation, and atherogenesis by disrupting the YAP/TAZ-BRD4 axis.","authors":"Praveen Krishna Veerasubramanian, Vijaykumar S Meli, Hamza Atcha, Wenqi Wang, Timothy L Downing, Wendy F Liu","doi":"10.1093/jleuko/qiag017","DOIUrl":"https://doi.org/10.1093/jleuko/qiag017","url":null,"abstract":"<p><p>Macrophage dysfunction is hallmark of atherosclerotic disease, characterized by inflammation and uptake of oxidized low-density lipoproteins (oxLDL). We investigate the role of the epigenetic reader bromodomain-containing protein 4 (BRD4) in orchestrating macrophage responses through interactions with the mechanosensitive transcriptional coactivators YAP/TAZ. Suppression of BRD4 via bromodomain and extra-terminal motif (BET) protein inhibitors (BETi) unveils a remarkable capacity to mitigate YAP/TAZ-driven inflammation. Knockdown of YAP, TAZ or BRD4 in macrophages shows a significant convergence of inflammatory genes under the regulatory purview of these transcriptional regulators. In addition, persistent activation of YAP and TAZ initiates a partial inflammatory phenotype in macrophages, which is effectively ameliorated with BETi. Notably, CD36 and low-density lipoprotein (LDL) receptor-1 (LOX1), pivotal receptors involved in uptake of oxidized low-density lipoprotein (oxLDL), emerge as direct YAP/TAZ targets. We employed a BD2-specific BETi, ABBV-744, in an AAV-PCSK9-induced atherosclerosis model to test the therapeutic potential of BET inhibition. Although reduction in cholesterol levels is modest, BETi substantially curtails plaque formation, diminishing macrophage infiltration, and suppressing the upregulation of YAP/TAZ and oxLDL uptake receptors associated with atherogenesis. Intriguingly, even in conditions marked by heightened YAP/TAZ expression induced by myeloid cell-targeted YAP/TAZ overexpression, BETi effectively dampens inflammation, mitigates foam cell formation, and disease progression. Our work underscores the considerable promise of targeting the YAP/TAZ-BRD4 axis as a therapeutic strategy for averting atherosclerosis, thereby disrupting the relentless cycle of inflammation, mechanosensory responses, and oxLDL uptake characteristic of atherosclerosis progression.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773776","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":"Macrophage and fibro-adipogenic progenitor (FAP) communication in skeletal muscle regeneration: Tissue homeostasis and pathogenic remodeling.","authors":"Seily Shrestha, Abbey Politeski, Sarah A Dick","doi":"10.1093/jleuko/qiag054","DOIUrl":"https://doi.org/10.1093/jleuko/qiag054","url":null,"abstract":"<p><p>Skeletal muscle regeneration depends on coordinated interactions between macrophages, fibro-adipogenic progenitors (FAPs), and muscle stem cells (MuSCs). Following injury, macrophages transition from pro-inflammatory to anti-inflammatory phenotypes, regulating debris clearance, cytokine secretion, and the activity of FAPs and MuSCs. FAPs transiently support MuSC-mediated regeneration but, if not cleared appropriately, differentiate into fibroblasts or adipocytes, contributing to fibrosis and fatty infiltration. Dysregulated macrophage-FAP crosstalk drives pathological conditions, including Duchenne Muscular Dystrophy (DMD) and age-related sarcopenia, where imbalances in cytokines and growth factors exacerbate maladaptive remodeling. FAP-derived colony-stimulating factor 1 (CSF1) sustains macrophage survival while macrophage-derived signals, including tumor necrosis factor alpha (TNF-α) and transforming growth factor beta (TGF-β), regulate FAP apoptosis, proliferation, and differentiation, shaping the regenerative niche. Single-cell and spatial transcriptomic approaches have revealed extensive heterogeneity among resident and infiltrating macrophages and FAP subsets, uncovering the molecular circuits underlying intercellular communication. Therapeutic strategies targeting cytokines and growth factors show promise in restoring balanced macrophage-FAP signaling, enhancing regeneration, and limiting fibrosis and fatty infiltration. Understanding the temporal dynamics of macrophage-FAP interactions is essential for developing interventions that preserve muscle homeostasis and counteract degenerative disease.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773792","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":"T cell exhaustion: Next-generation target of autoimmune diseases?","authors":"Yuzhen Ouyang, Mengchuan Luo, Kailin Li, Kangzhi Chen, Zeyi Wen, Qian Zhou, Guanzhong Shi, Siyu Xu, Zhaohui Luo, Huan Yang","doi":"10.1093/jleuko/qiag052","DOIUrl":"https://doi.org/10.1093/jleuko/qiag052","url":null,"abstract":"<p><p>Exhausted T cells (Tex), characterized by impaired cytotoxic function, play a detrimental role in anti-tumor and anti-infection immunity but represent promising therapeutic targets for autoimmune diseases. Persistent exposure to auto-antigens drives autoreactive CD8+ or CD4+T cells toward an exhausted state, thereby mitigating excessive damage to healthy tissues. Inducing T cell exhaustion may offer a targeted approach to suppress pathological autoimmunity. In this review, we describe the markers, characteristics, and developmental phases of T cell exhaustion, discuss its close association with autoimmune diseases, and highlight Tex as a potential biomarker. We also summarize Tex-targeted therapeutic strategies, including inhibitory receptor activation, TCR overstimulation, and metabolic intervention, to provide insights for future treatments. The clinical translation gap of Tex-targeted therapy has also been proposed from stability, safety, and disease-specific considerations. Although challenges remain in areas such as antigen specificity and tenuous tolerance, therapies targeting Tex hold considerable potential to disrupt pathogenic circuits, realize disease remission, and reduce the risk of relapse in autoimmune diseases.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773849","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":"Macrophage heterogeneity influences cellular response to HIV infection and latency modulation.","authors":"Michelle E Wong, Laura Rikard-Bell, Salimeh Ebrahimnezhaddarzi, Morgane Brunton-O'Sullivan, Betty Kouskousis, Mark Ziemann, Anthony Jaworowski, Anna C Hearps","doi":"10.1093/jleuko/qiag053","DOIUrl":"https://doi.org/10.1093/jleuko/qiag053","url":null,"abstract":"<p><p>HIV reservoirs persist in macrophages in people with HIV despite antiretroviral therapy, representing a barrier to cure. Factors which govern the establishment and reversal of HIV latency in different macrophage types remain poorly understood. An in vitro HIV latency model was used to investigate infection in human monocyte-derived macrophages (MDM), alveolar-like MDM (AlvMDM) and monocyte-derived microglia (MDMi). HIV infection and latency reactivation were similar between MDM and AlvMDM, whilst MDMi showed low susceptibility to HIV infection and minimal latent infection. Polarization of MDM and AlvMDM with M2-, but not M1-, inducing cytokines enhanced HIV reactivation, whilst TLR stimulation inhibited HIV reactivation in latently-infected AlvMDM, but not MDM. Single cell RNA-seq analysis identified non-productively infected macrophages expressing HIV RNA transcripts, consistent with latently-infected cells. Latently-infected MDM and AlvMDM exhibited upregulated expression of genes encoding cell surface receptors including MERTK and the immune checkpoint molecule CD137, respectively. Purification of non-productively infected AlvMDM with high CD137 expression enriched for cells with higher HIV DNA content. Substantial differences were observed between macrophage types in both the extent and nature of transcriptional changes in response to latent and productive infection, with HIV infection having a greater impact on AlvMDM as compared to MDM. These findings highlight significant differences between macrophage types regarding their susceptibility to latency modulation and response to HIV infection. Further, we identify unique transcriptional changes in latently-infected, monocyte-derived macrophages which differ by macrophage type. These findings have implications for the development of strategies to target latently-infected tissue macrophages for HIV elimination.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773799","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":"Guidelines for single cell RNA sequencing analysis of eosinophils.","authors":"Kristina Handler, Alessandra Gurtner, Deeksha Raju, Ignacio Gonzalez Perez, Isabelle C Arnold","doi":"10.1093/jleuko/qiag055","DOIUrl":"https://doi.org/10.1093/jleuko/qiag055","url":null,"abstract":"<p><p>Eosinophils are challenging to profile by single cell RNA sequencing (scRNA-seq) approaches due to their fragile nature and the abundance of RNases and cytotoxic enzymes stored in cytoplasmic granules, which can compromise RNA integrity upon stress. Although recent technical advances have improved eosinophil recovery, their transcriptomes remain intrinsically sparse, particularly in mature cells, resulting in low gene detection and high dropout rates that can bias standard preprocessing and quality-control steps.  Here, we integrated multiple publicly available eosinophil scRNA-seq datasets from our laboratory and other groups, and performed comparative analyses across platforms, tissues, and species. We show that eosinophils consistently display among the lowest transcriptome coverage, emphasizing the need for eosinophil-adapted analytical strategies. To enable reliable eosinophil annotation despite high dropout rates, we curated a dedicated eosinophil marker-gene panel derived from cross-dataset differential expression signatures. We further demonstrate that intron-inclusive genome alignment markedly increases eosinophil gene and transcript detection compared with exon-only alignment. Finally, we identify genotype-dependent programs: Il5-transgenic eosinophils exhibit a less mature profile, whereas wild-type eosinophils show stronger host-defense-associated signatures. Together, these results provide a practical framework for eosinophil-focused scRNA-seq analysis that improves eosinophil recovery, annotation, and biological interpretation in complex datasets.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773815","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":"CD177 Promotes NLR Inflammasome Activation in Acute Respiratory Distress Syndrome by Remodeling Neutrophil Glycolytic Metabolism.","authors":"Dongfeng Shen, Yuejiao Sun, Yixin Xu, Yahong Sun, Xiaolong Ma","doi":"10.1093/jleuko/qiag051","DOIUrl":"https://doi.org/10.1093/jleuko/qiag051","url":null,"abstract":"<p><p>Acute respiratory distress syndrome (ARDS) is a high-mortality lung disorder driven by excessive neutrophil activation. While neutrophils are central to ARDS, the metabolic pathways fueling their inflammatory response remain unclear. This study identifies CD177 as a critical regulator of neutrophil glycolysis and NLRP3 inflammasome activation. Bioinformatics and animal models show that elevated CD177 correlates strongly with increased lactate and IL-1β levels. In vitro experiments demonstrate that CD177 knockdown reduces glycolytic flux and suppresses IL-1β release, a process reversed by lactate supplementation. Furthermore, treating ARDS mice with anti-CD177 antibodies significantly reduces pulmonary edema and tissue injury. These results establish the CD177-glycolysis-NLRP3 axis as a major driver of lung inflammation. Targeting this metabolic checkpoint provides a promising strategy for treating ARDS.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773789","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":"Uncovering the gut-immune-joint axis: causal links between gut Microbiota, immune cells, and osteoarthritis.","authors":"Yuxi Liu, Zhilei Zhang, Bing Zhao, Jingang Song, Chao Wei","doi":"10.1093/jleuko/qiag042","DOIUrl":"10.1093/jleuko/qiag042","url":null,"abstract":"<p><p>Gut microbiota have been increasingly implicated in osteoarthritis (OA), but causal pathways remain unclear. Using the Gut-Immune-Joint Axis framework, we analyzed publicly available genome-wide association study (GWAS) summary statistics from one primary and 2 secondary datasets to evaluate genetically predicted associations between gut microbiota and OA and to test immune cells as potential mediators. Bidirectional Mendelian randomization (MR) identified 5 bacterial genera genetically associated with OA in the primary dataset, with no evidence of reverse causality. Two-step MR highlighted Bilophila and the immune cell subtype CD45 on CD33dim HLA DR + CD11b- as being associated with OA (P < 0.05), and multivariable MR suggested partial mediation by this immune cell (20.0%, P = 0.003). In secondary analyses, 2 genera were associated with knee OA (KOA) and 5 with hip OA (HOA), again without reverse genetic effects. Terrisporobacter, the HLA DR + CD4 + to T-cell ratio, and the HLA DR + CD4 + to lymphocyte ratio were associated with KOA (all P < 0.05), with mediation by the HLA DR + CD4 + to T-cell ratio (-12.0%, P = 0.001). Roseburia and Myeloid DC AC were associated with HOA (all P < 0.05). Collectively, these findings support causal links between specific gut microbial genera and OA and implicate immune-cell traits as mediators, strengthening the gut-immune-joint axis concept and highlighting potential therapeutic targets.</p>","PeriodicalId":16186,"journal":{"name":"Journal of Leukocyte Biology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2026-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512576","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}