Frontiers in Immunology最新文献

{"title":"Hypoxia-inducible factor-1α-mediated metabolic reprogramming in sepsis-associated organ dysfunction: organ-specific metabolic mismatch and therapeutic perspectives.","authors":"Yuge Wu, Jiantao Lu, Yue Mo, Yaoqi Xu, Xiaoxi Yan, Caifen Yan, Yingzhen Wang","doi":"10.3389/fimmu.2026.1998563","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1998563","url":null,"abstract":"<p><p>Sepsis-associated organ dysfunction arises from immune dysregulation, heterogeneous microcirculatory perfusion, impaired oxygen utilization, and cellular metabolic disturbances. Hypoxia-inducible factor-1α (HIF-1α) links oxygen sensing and inflammatory signaling to substrate use and mitochondrial function, but its effects vary with cell type, organ energy demand, and disease stage. This review uses metabolic flexibility and organ-specific metabolic mismatch to integrate these differences. Metabolic flexibility denotes the capacity to adjust energy-producing pathways during stress and restore efficient oxidative metabolism after stress subsides; mismatch develops when cellular energy production no longer meets immediate organ function or repair requirements. HIF-1α-related glycolysis supports early antimicrobial responses in myeloid cells and short-term hypoxic tolerance in some parenchymal cells. Persistent glycolysis combined with restricted pyruvate and fatty acid oxidation and impaired mitochondrial renewal may instead prolong inflammation and limit barrier repair, tubular transport, myocardial contraction, hepatic clearance, and neurological recovery. Differences among the lungs, kidneys, heart, intestine, liver, and brain indicate that global HIF activation or inhibition is unlikely to produce uniform benefit. Cell type-resolved localization, dynamic metabolic flux, mitochondrial function, and organ-level endpoints are therefore required to distinguish adaptive reprogramming from persistent bioenergetic dysfunction and to guide phase-matched metabolic intervention.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1998563"},"PeriodicalIF":7.0,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13697615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated proteomic and metabolomic profiling characterizes tryptophan metabolic disturbance associated with mortality in ICU-admitted SFTS patients.","authors":"Li Chen, Puhui Liu, Chuanzhen Niu, Chenxiao Hao, Fengxue Zhu, Guangjie Wang, Huiying Zhao","doi":"10.3389/fimmu.2026.1898053","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1898053","url":null,"abstract":"<p><p>Severe fever with thrombocytopenia syndrome (SFTS), caused by Dabie bandavirus, is associated with high mortality among intensive care unit (ICU) patients; however, the integrated proteomic-metabolomic mechanisms underlying fatal outcomes remain poorly characterized. This prospective cohort study enrolled 68 patients with SFTS, who were admitted to the ICU and classified them as survivors (n = 33) or non-survivors (n = 35) according to their 28-day clinical outcomes. Untargeted metabolomic profiling using ultra-high-performance liquid chromatography-tandem mass spectrometry and quantitative proteomic profiling using data-independent acquisition mass spectrometry were performed on plasma samples collected at ICU admission. Multivariable analysis, pathway enrichment analysis, correlation analysis, and receiver operating characteristic (ROC) curve analysis were used to identify potential prognostic biomarkers and characterize molecular associations. Non-survivors exhibited more severe multi-organ injury and systemic inflammation. Metabolomic profiling revealed marked disruption of tryptophan metabolism: L-tryptophan levels were decreased, whereas kynurenine and its downstream metabolites (kynurenic acid [KA], 3-hydroxyanthranilic acid [3-HAA], xanthurenic acid [XA], and 5-hydroxyindolepyruvate [5-HIP]) were increased, suggesting activation of the kynurenine pathway. The four core tryptophan metabolites yielded a combined area under the curve (AUC) of 0.934 for predicting 28-day mortality and were correlated with indicators of renal function and coagulation. Proteomic profiling identified 200 differentially expressed proteins: proteins upregulated in survivors were enriched in the proteasome pathway, whereas those upregulated in non-survivors were enriched in the IL-17 pathway and other inflammatory and immune pathways. Integrated analysis revealed that the four tryptophan metabolites were associated with 20 differentially expressed proteins, six of which showed robust associations within outcome subgroups. Collectively, tryptophan metabolic disturbances coupled with inflammatory proteomic features may characterize fatal severe SFTS, and the identified metabolite-protein signatures may serve as promising prognostic biomarkers and potential therapeutic targets in critically ill patients.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1898053"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149244249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Context dependent interactions between protozoan infections and cancer biology-a retrospective review.","authors":"Fanglei Yu, Zheng Wu, Yaru Huang, Xiaochen Qi, Jun Wu, Yuanhua Qin","doi":"10.3389/fimmu.2026.1968151","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1968151","url":null,"abstract":"<p><p>Protozoan infections can influence tumor biology through immune modulation, effects on tumor cells and vasculature, and changes in mucosal homeostasis. The supporting evidence, however, differs substantially among organisms and experimental settings. Selected studies of Toxoplasma gondii, Plasmodium species, and Trypanosoma cruzi demonstrate tumor suppression in cell and animal models, including immune activation, altered myeloid-cell function, and inhibition of angiogenesis. Associations between intestinal or urogenital protozoa and human cancers are mainly observational and do not establish carcinogenesis. Malaria associated with Plasmodium falciparum in holoendemic areas provides a distinct cancer-associated context that cannot be equated with experimental antitumor interventions. This narrative review distinguishes population associations, mechanistic observations, causal evidence within experimental models, and human therapeutic investigation. It evaluates strain or subtype, infection burden and duration, tissue tropism, host immune status, and observation timing as candidate modifiers rather than universally validated determinants. Direct tumor-cell effects, vascular effects, and host-immune-mediated effects are considered separately. Particular attention is given to inconsistent Trichomonas vaginalis and Blastocystis findings, limitations of murine models, confounding and reverse causation, and the safety of live-organism approaches in immunocompromised patients. Registered Plasmodium-based oncology studies demonstrate clinical investigation, but registration does not establish therapeutic benefit. Most engineered parasites and parasite-derived platforms discussed remain preclinical. The proposed framework organizes heterogeneous evidence and identifies testable questions for safer translational research; it does not imply that natural protozoan infection provides a predictable clinical benefit.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1968151"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13691939/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut microbiota-mediated tryptophan metabolic dysregulation in the comorbidity of inflammatory bowel disease and autism spectrum disorder: mechanisms and research progress.","authors":"Mingyu Lu, Yuxuan Chen, Hengli Zhou, Yingzhuo Lin","doi":"10.3389/fimmu.2026.1950055","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1950055","url":null,"abstract":"<p><p>The \"microbiota-gut-brain axis\" represents a critical link connecting various aspects of intestinal physiology, brain function, and behavioral performance. Among these, tryptophan metabolism abnormalities mediated by gut microbes through the gut-brain axis (GBA) have garnered widespread attention in the study of IBD-ASD comorbidity. This article reviews the current state of research on tryptophan metabolism abnormalities in IBD-ASD comorbidity, with a particular focus on the connection between peripheral and central tryptophan metabolic derangements mediated by gut microbes via the GBA. Furthermore, we summarize and analyze potential therapeutic targets and intervention strategies in this comorbid condition, integrating recent mechanistic studies and clinical evidence to provide a conceptual framework for understanding the potential mechanisms underlying IBD-ASD comorbidity. However, direct evidence from patients with confirmed IBD-ASD comorbidity remains limited at present, and further clinical studies are still needed to test this hypothesis.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1950055"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13692640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute lung injury: an integrated view of molecular drivers, immune dysregulation, and emerging therapeutic strategies.","authors":"Aihua Wang, Haizhao Liu, Chengfen Yin, Yawen Song, Yue Jin, Lei Xu, Siwei Wang, Jiaxin Li, Xiping Guo, Yongli Ma, Yutong Jin, Wei Liu, Ximo Wang","doi":"10.3389/fimmu.2026.1937966","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1937966","url":null,"abstract":"<p><p>Acute lung injury (ALI, a term widely used in preclinical animal studies, while the clinical definition of ALI was eliminated in the Berlin criteria) and its severe human clinical counterpart, acute respiratory distress syndrome (ARDS), constitute life-threatening clinical syndromes characterized by diffuse alveolar damage, pulmonary edema, and severe hypoxemia. These conditions are associated with dismal mortality rates and significantly impair patient survival and recovery. Over the past decades, advancements in critical care medicine and molecular biology have deepened our understanding of the pathological mechanisms underlying ALI and ARDS. Aberrantly activated signaling pathways and molecular and cellular events have emerged as key elements to decipher core pathogenic processes, identify early biomarkers, and develop novel therapeutic strategies. This review aims to provide a comprehensive overview of ALI and ARDS, encompassing their definition, historical context, epidemiology, and common etiological factors, with a focus on recent advances in pathological mechanisms, signaling pathways, epigenetic regulation, and therapeutic interventions. Treatment approaches include lung-protective ventilation, fluid management, targeted pharmacotherapy, mesenchymal stromal cell therapy, and nanomaterial-based delivery systems. These developments offer valuable insights into the complex mechanisms of preclinical ALI and human ARDS and contribute to the advancement of clinical diagnosis and treatment.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1937966"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13693559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Candidate molecular endotypes and dynamic risk prediction in anti-MDA5-positive dermatomyositis-associated interstitial lung disease: a systematic scoping review.","authors":"Zhiwei Zuo, Jianguo Yang, Jianbin Li, Renhe Li, Wei Liu","doi":"10.3389/fimmu.2026.1979138","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1979138","url":null,"abstract":"<p><strong>Background: </strong>Anti-melanoma differentiation-associated protein 5 antibody-positive dermatomyositis (anti-MDA5+ DM) spans pulmonary states from no detectable interstitial lung disease (ILD) to rapidly progressive ILD (RP-ILD). We mapped molecular programs and prediction evidence to determine how recurrent biological states may support dynamic stratification.</p><p><strong>Methods: </strong>PubMed, Web of Science, Ovid and Embase were searched from inception to 22 August 2026. Two reviewers independently screened records and extracted data. Reporting followed PRISMA-ScR; evidence was synthesized across molecular and prediction domains.</p><p><strong>Results: </strong>Of 4, 166 records, 2, 317 remained after deduplication, 349 underwent full-text assessment, and 95 sources (80 primary studies and 15 syntheses) were included. Type I/III interferon signaling was the most reproducible program. Myeloid inflammatory-remodeling, adaptive activation with lymphocyte or natural-killer-cell loss, vascular-coagulation injury, and immunometabolic disturbance formed additional overlapping axes aligned with pulmonary-state transitions. Clinical and radiomic models showed strong short-term discrimination; harmonized landmarks, calibration, geographic validation, and decision-timed molecular sampling would strengthen clinical use.</p><p><strong>Conclusion: </strong>The evidence supports an integrated map linking recurrent molecular programs to dynamic pulmonary risk. A calibrated clinical-imaging backbone, augmented by parsimonious molecular modules with incremental value and updated at prespecified landmarks, offers a practical framework for prospective endotype validation and treatment-aware prediction in anti-MDA5+ DM-ILD.</p><p><strong>Systematic review registration: </strong>https://doi.org/10.37766/inplasy2026.10.0018, identifier INPLASY2026100018.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1979138"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149244064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exercise, physical activity, and physical fitness in psoriasis and psoriatic arthritis: an umbrella review.","authors":"Zikun Lyu, Jingshi Ma, Chenzhe Ma, Xuechen Tian, Liye Liu, Jiayi Zhang, Yafei Gao","doi":"10.3389/fimmu.2026.1921728","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1921728","url":null,"abstract":"<p><strong>Background: </strong>Exercise, physical activity, and physical fitness are increasingly discussed in psoriasis and psoriatic arthritis (PsA), but the evidence base is uneven: intervention reviews predominantly concern PsA, whereas evidence for cutaneous psoriasis is largely observational or embedded in broader lifestyle interventions.</p><p><strong>Methods: </strong>This systematic review was conducted as an umbrella review of intervention effects and observational exposure-outcome associations. The protocol was registered in PROSPERO (CRD420261403713). PubMed, Web of Science, Embase, Cochrane Library, Scopus, and SPORTDiscus were searched from inception to 1 March 2026. Two reviewers independently screened records and extracted data, with disagreements resolved by discussion and, when necessary, a third reviewer. Reporting followed PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) 2020 and PRIOR (Preferred Reporting Items for Overviews of Reviews). AMSTAR 2 (A Measurement Tool to Assess Systematic Reviews 2), corrected covered area (CCA), GRADE (Grading of Recommendations, Assessment, Development and Evaluations), and the Ioannidis credibility classification were applied as appropriate.</p><p><strong>Results: </strong>Nine reviews were included. Eight reviews provided PsA evidence, including interventional, descriptive, or observational findings; one observational meta-analysis concerned prevalent cutaneous psoriasis. No eligible review isolated the effect of exercise on cutaneous-psoriasis severity. Overall confidence was Moderate for one review, Low for five, and Critically Low for three. No umbrella-level pooling was undertaken because the same trials recurred across reviews, particularly in the high-intensity interval-training/cardiorespiratory cluster (CCA approximately 16.7%), and populations, outcomes, comparators, and effect measures were heterogeneous. Vigorous activity (RR 0.76, 95% CI 0.67 to 0.85) and regular exercise frequency (RR 0.88, 95% CI 0.82 to 0.95) were associated with lower psoriasis prevalence, both with suggestive credibility. In PsA, possible improvements in fitness, disease activity, pain, function, and body composition were based mainly on single small trials and had very low certainty.</p><p><strong>Conclusion: </strong>The evidence differs by disease. For cutaneous psoriasis, current findings are observational and do not establish an exercise effect on disease severity or incidence. For PsA, intervention findings are sparse, duplicated across reviews, and of very low certainty. Safety reporting was incomplete and did not permit a disease-specific conclusion. Adequately powered, prospectively registered trials with disease-specific outcomes and systematic adverse-event reporting are required.</p><p><strong>Systematic review registration: </strong>https://www.crd.york.ac.uk/PROSPERO/, identifier CRD420261403713.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1921728"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149244113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TCR clonotyping of paired blood and tonsillar T-follicular cells reveals the mixed origin of CD38^high Tfrs.","authors":"Sophiya R Sokolova, Vladimir A Grigoriants, Irina A Shagina, Ekaterina V Barsova, Maria A Nomerovskaya, Jamilya Z Khalifaeva, Alexander V Gurov, Olga V Britanova, Ivan V Zvyagin, Dmitriy M Chudakov, Irina L Grigorova","doi":"10.3389/fimmu.2026.1947623","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1947623","url":null,"abstract":"<p><p>Circulating T follicular regulatory (cTfr) cells are measured as blood biomarkers after vaccination, in autoimmune disease (e.g., lupus, rheumatoid arthritis) and cancer immunotherapy, yet whether they originate from natural Tregs (yielding nTfr) or germinal center T follicular helper (GC Tfh) cells (yielding iTfr) remains unknown. This distinction is critical for interpreting cTfr expansion as Treg-derived regulation versus Tfh-derived negative feedback. To characterize tonsillar follicular T cell heterogeneity and resolve the origins of cTfr cells we applied single-cell multiomics and bulk T cell receptor sequencing (TCRβ-seq) analysis of matched human tonsil and blood. Tonsillar nTfr and iTfr cells distribute across shared transcriptional states, with <i>CD38</i> expression distinguishing iTfr from nTfr in most contexts. However, within a transitional cluster positioned between activated Tfh and Tfr cells, nTfr-like cells also upregulated CD38, indicating that its specificity for iTfr is not absolute. Peripheral blood CD38^- cTfr cells shared clonotypes exclusively with non-follicular Tregs and lacked overlap with GC Tfh, indicating predominantly Treg origin. CD38^high cTfr cells captured a mixed population: some shared clonotypes with tonsillar GC Tfh (iTfr), while others shared clonotypes with non-follicular Tregs (nTfr). These findings establish that accurate discrimination of iTfr versus nTfr within the CD38^high compartment requires TCR clonal reference to matched tissue.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1947623"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149244195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanoinflammation in osteoarthritis: knowledge evolution, cellular interactions, and translational research priorities.","authors":"Bo Wang, Yuge Li, Jiaxing Huang, Yin Lian, Lina Gao, Suya Zhang, Sijin Tang, Dandan Li, Renxuan Yang, Huai Wu","doi":"10.3389/fimmu.2026.1955650","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1955650","url":null,"abstract":"<p><strong>Background: </strong>Osteoarthritis (OA) is increasingly recognized as a whole-joint disorder in which mechanical stress, cellular mechanosensing, and inflammatory responses interact across joint tissues. Although OA mechanoinflammation has attracted growing attention, its literature remains distributed across mechanobiology, inflammation research, molecular medicine, and translational research. This study aimed to map the knowledge structure and temporal development of OA mechanoinflammation and to characterize relationships among mechanosensing, inflammatory responses, tissue crosstalk, and emerging research priorities.</p><p><strong>Methods: </strong>Publications related to OA mechanoinflammation were retrieved from the Web of Science Core Collection and PubMed from January 1, 2000 to May 23, 2026. Bibliometric and knowledge-map analyses characterized publication trends, collaboration patterns, reference co-citation structures, author keyword themes, journal-level knowledge flows, and sensitivity to database source, retrieval dependence, and clustering parameters. Keyword-reference correspondence was evaluated using year-stratified permutation testing and bootstrap confidence intervals, and temporal use of reference clusters was assessed using an annual citation-opportunity-adjusted analysis.</p><p><strong>Results: </strong>Research output increased markedly in recent years. Under the primary analytical configuration, reference co-citation and author keyword analyses each yielded four interpretable intermediate-resolution domains. Validated keyword-reference correspondence identified selective relationships linking mechanotransduction-related themes with the mechanical-loading and mechanosensitive-channel knowledge bases, together with a significant relationship between the broader inflammatory-degeneration theme and contemporary OA pathogenesis, aging, and tissue crosstalk. After adjustment for citation opportunity, recent years showed greater relative use of the contemporary OA/tissue-crosstalk and mechanosensitive-channel reference domains, with substantial year-to-year heterogeneity. Sensitivity analyses showed high stability of the principal reference-based structures and identified greater variability at keyword-domain boundaries.</p><p><strong>Conclusions: </strong>OA mechanoinflammation is an expanding interdisciplinary research area linking mechanical context, cellular mechanosensing, inflammatory responses, and whole-joint remodeling at the literature level. The mapped structures and recent temporal patterns identify testable priorities for multimodal phenotyping, biomarker validation, mechanistically relevant models, and combined mechanical-inflammatory intervention research. These translational directions remain hypothesis-generating and require prospective experimental and clinical validation.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1955650"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13690958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: New insights into roles of IL-7R gene as a diagnostic biomarker for post-stroke depression.","authors":"Mengyu Liu, Haochen Sun, Qun Yao, Duohao Wang, Jihong Zhang, Xing Ye, Xinyang Qi","doi":"10.3389/fimmu.2026.2000379","DOIUrl":"https://doi.org/10.3389/fimmu.2026.2000379","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fimmu.2024.1506214.].</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"2000379"},"PeriodicalIF":7.0,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13693555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149265822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}