Frontiers in Immunology最新文献

{"title":"Atherosclerosis features in rheumatic diseases - focus on peripheral artery disease.","authors":"Alexandr Ceasovschih, Alina Dima, Javier Rodriguez-Carrio, Anastasia Balta, Raluca-Elena Alexa, Bianca Codrina Morarasu, Catalina Lionte, Fotios Barkas, Maciej Banach, Victorita Sorodoc, Laurentiu Sorodoc","doi":"10.3389/fimmu.2026.1814953","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1814953","url":null,"abstract":"<p><p>Rheumatic and musculoskeletal diseases (RMDs) confer an increased cardiovascular risk beyond traditional factors, with peripheral artery disease (PAD) being an important source of morbidity and disability in these patients. This review summarizes current evidence on PAD across RMDs, including rheumatoid arthritis, systemic lupus erythematosus, antiphospholipid syndrome, systemic sclerosis, polymyalgia rheumatica, psoriatic arthritis, and primary Sjögren's syndrome. Physiopathological mechanisms involved include persistent inflammation, immune dysregulation, and the presence of pathogenic autoantibodies. Protective humoral responses have also been linked to reduced CV risk and may serve as future biomarkers. Clinical studies reveal variable PAD prevalence across diseases but consistent high underdiagnosis. Optimal management requires aggressive CV risk control, including lipid-lowering, immunomodulatory, and biologic therapies. This review underscores PAD as a distinct and clinically relevant manifestation of systemic autoimmunity, calling for targeted screening and prevention strategies in rheumatic populations.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1814953"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836826","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":"Multi-omics insights into SERPINE2-driven post-metastatic microenvironmental reprogramming in advanced cancers: implications for molecular targeting and immunotherapy.","authors":"Ying Yi, Jianhong Lai, Peng Zhang, Rong Zhang","doi":"10.3389/fimmu.2026.1815463","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1815463","url":null,"abstract":"<p><p>Metastasis remains the primary cause of cancer-related mortality, driven not only by intrinsic genetic alterations but also by dynamic reprogramming of the post-metastatic microenvironment. Recent advances in multi-omics technologies-including single-cell transcriptomics, spatial profiling, methylome analysis, chromatin architecture mapping, and proteomics-have reshaped our understanding of metastatic ecosystems and revealed key regulatory nodes that coordinate tumor progression. Among these, SERPINE2 has emerged as a convergent mediator across diverse cancer types. Multi-layered evidence demonstrates that SERPINE2 integrates tumor-intrinsic signaling and microenvironmental remodeling. Mechanistically, SERPINE2 stabilizes oncogenic receptors such as EGFR by inhibiting ubiquitination-dependent degradation, sustains downstream STAT3/ERK activation, and enhances DNA damage response through ATM phosphorylation and homologous recombination repair. Concurrently, as a secreted factor, SERPINE2 promotes cancer-associated fibroblast activation, M2 macrophage polarization, extracellular matrix remodeling, and angiogenesis, collectively fostering immune suppression and metastatic persistence. These dual tumor-intrinsic and stromal functions position SERPINE2 as a molecular hub in post-metastatic adaptation. Targeting SERPINE2 may therefore represent a paradigm shift in advanced cancer therapy by simultaneously disrupting oncogenic persistence, genome maintenance, and immune exclusion. This review synthesizes multi-omics insights into SERPINE2-driven microenvironmental reprogramming and discusses emerging therapeutic strategies integrating molecular targeting and immunotherapy in metastatic cancers.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1815463"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836850","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":"Skeletal muscle as a dynamic immunological niche for vaccination.","authors":"Moataz Noureddine, Michael Schotsaert","doi":"10.3389/fimmu.2026.1808541","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1808541","url":null,"abstract":"<p><p>Intramuscular vaccination has long been a cornerstone of preventive medicine and has substantially reduced global mortality from infectious disease. As vaccine development has expanded to address increasingly complex targets, including chronic infections and cancer, it has become clear that vaccine efficacy depends not only on antigen design but also on the inflammatory and cellular cues present at the site of delivery. Despite this, the skeletal muscle-the most common site of vaccine administration-has received comparatively little attention as an immunological environment. Skeletal muscle is a highly dynamic, regenerative tissue whose immune composition is actively remodeled by injury, aging, and disease. How these context-dependent immune states shape vaccine uptake and downstream immune responses remains poorly understood. In this review, we examine the immune landscape of skeletal muscle in health and disease and discuss how its intrinsic regenerative programs, and their disruption in conditions such as sarcopenia, may influence intramuscular vaccine responses.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1808541"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836897","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":"Multi-omics analysis of ST3GAL4-mediated lacto/neolacto glycosphingolipid metabolism reveals immune evasion and poor prognosis in TNBC.","authors":"Yu Zhang, Shuhan Wang, Xudong Yu, Kang Sun, Shengying Wang","doi":"10.3389/fimmu.2026.1760560","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1760560","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is a highly aggressive subtype lacking effective targeted therapies. Increasing evidence highlights metabolic reprogramming as a hallmark of tumor progression and immune evasion. However, in this context, the specific metabolic-immune mechanisms underlying TNBC remain unclear.</p><p><strong>Methods: </strong>We performed an integrative multi-omics analysis combining bulk RNA-seq, single-cell RNA-seq, and spatial transcriptomics across TNBC and non-TNBC samples from TCGA, GEO, and 10X Genomics. Eighty-five KEGG metabolic pathways were profiled to identify TNBC-specific alterations. Machine learning models (Random Forest, XGBoost) were used to prioritize key metabolic genes. Immune infiltration was evaluated using CIBERSORT, ssGSEA, and ESTIMATE algorithms. Validation was conducted through immunohistochemistry (IHC) on 100 clinical samples from The First Affiliated Hospital of Anhui University Chinese Medicine.</p><p><strong>Results: </strong>The Lacto/Neolacto glycosphingolipid metabolism pathway was markedly activated in TNBC compared to adjacent and non-TNBC tissues, correlating with worse prognosis. Machine learning identified ST3GAL4 as the core enzyme within this pathway. High ST3GAL4 expression was associated with increased infiltration of regulatory T cells (Tregs) and M2 macrophages, reduced CD8⁺ T-cell activity, and enhanced epithelial-mesenchymal transition. Spatial transcriptomics confirmed localized enrichment of immunosuppressive cells in ST3GAL4-high regions. IHC validation demonstrated that ST3GAL4 overexpression in TNBC tissues predicts poor clinical outcomes.</p><p><strong>Conclusions: </strong>ST3GAL4-driven glycosphingolipid metabolism promotes tumor immune evasion and aggressiveness in TNBC. This metabolic-immune coupling axis represents a potential therapeutic target, offering mechanistic rationale for combining metabolic and immune checkpoint blockade strategies.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1760560"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836909","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":"Unilateral facial palsy with hemiplegia and positive anti-GT1a antibody: a case report and literature review.","authors":"Fangfang Wang, Jing Miao","doi":"10.3389/fimmu.2026.1793550","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1793550","url":null,"abstract":"<p><strong>Background: </strong>Guillain-Barré syndrome (GBS) is an autoimmune-mediated disorder characterized by an acute onset of symmetrical flaccid limb weakness. However, cases of persistent unilateral limb weakness and facial palsy with anti-GT1a antibody positivity have been rarely reported. Here, we describe this case to highlight its clinical importance.</p><p><strong>Case: </strong>A 60-year-old man presented with right shoulder and upper back pain, followed by right-sided limb weakness, peripheral facial paralysis, distal sensory impairment, and dyspnea. Symptoms were preceded by upper respiratory infection. Cerebrospinal fluid showed albuminocytological dissociation. Electromyography reported peripheral nerve damage in the extremities. Serum anti-GT1a IgG was positive. After a five-day course of intravenous immunoglobulin, he showed marked recovery in motor, sensory, and respiratory function. At six-month follow-up, his symptoms except dyspnea basically returned to normal.</p><p><strong>Conclusion: </strong>This case suggests a potential distinct GBS phenotype featuring unilateral limb weakness, unilateral facial palsy, and anti-GT1a antibody positivity, with a good response to IVIG. These findings expand the clinical spectrum of GBS and emphasize recognizing unilateral presentations to prevent misdiagnosis.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1793550"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836962","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":"Continuous antiretroviral therapy induces progressive senescence-like reprogramming of alveolar macrophages.","authors":"Vinicius M Fava, Monica Dallmann-Sauer, Marianna Orlova, Wilian Correa-Macedo, Ron Olivenstein, Cecilia Theresa Costiniuk, Jean-Pierre Routy, Luis B Barreiro, Erwin Schurr","doi":"10.3389/fimmu.2026.1805936","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1805936","url":null,"abstract":"<p><strong>Introduction: </strong>Advances in antiretroviral therapy (ART) have substantially improved the lives of people with HIV (PWH) and reduced HIV acquisition through pre-exposure prophylaxis (PrEP). However, the long-term effect of ART on the physiological state of cells remains poorly understood and PWH are currently suffering from a disproportionate burden of non-AIDS comorbidities, including lung diseases.</p><p><strong>Methods: </strong>Given the central function of alveolar macrophages (AM) in pulmonary immunity, we evaluated the impact of ART on AM of PWH and people on PrEP using a systems immunology approach.</p><p><strong>Results: </strong>We showed that continuous ART induces a progressive senescence-like pro-inflammatory state in AM characterized by increased constitutive epigenetic and transcriptomic priming of genes involved in cell-cycle arrest and senescence. At the AM single nucleus level, we discovered a coordinated gene regulatory network linking key pro-inflammatory transcription factors to the alterations induced by ART. The senescence ART-linked changes were strongly dependent on the duration of ART and irrespective of HIV infection. A secondary time independent ART-effect was observed for interferon signaling which impaired the AM response to ex vivo challenge with SARS-CoV-2.</p><p><strong>Discussion: </strong>Our data indicated that continuous ART promoted a dysregulated physiological state in AM. The results of our study advocate for optimized or adjuvant therapies to mitigate potential long-term adverse ART-effects.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1805936"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836511","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":"NeoTCRseek: an integrated platform for high-sensitivity identification of neoantigen-specific TCR clonotypes to track clinical T-cell dynamics.","authors":"Bin Song, Geng Liu, Bo Li, Yong Hou, Leo J Lee","doi":"10.3389/fimmu.2026.1674427","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1674427","url":null,"abstract":"<p><strong>Introduction: </strong>Identifying neoantigen-specific T-cell receptor (neoTCR) clonotypes is crucial for tracking clinical T-cell dynamics in personalized cancer immunotherapy. Despite advances in experimental and computational approaches for identifying antigen-specific TCR (asTCR) clonotypes, the identification of neoTCR clonotypes remains challenging due to their low frequencies and the limited sensitivity of current methods.</p><p><strong>Methods: </strong>We introduce NeoTCRseek, an integrated platform that combines extended T-cell culture, deep TCR sequencing, and advanced TCR-clustering tools to enhance neoTCR clonotype identification. NeoTCRseek was developed using a model cytomegalovirus (CMV) antigen and subsequently validated under two neoantigen setups: a single neoantigen and a neoantigen pool representing a multi-antigen context. For each antigen setup, we used three cell sorting-based methods to detect enriched clonotypes and built a validation dataset for asTCR clonotype characterization and NeoTCRseek performance evaluation.</p><p><strong>Results: </strong>NeoTCR clonotypes exhibited a significantly higher proportion of low-frequency clonotypes (0.01%-0.1%) than CMV-specific ones (70.3% vs. 33.3%). Nonetheless, NeoTCRseek achieved a detection limit of 0.01% and high accuracy in both single- and multi-antigen contexts by integrating expanded clonotype detection with co-clustering-based TCR prediction. Compared with the benchmark, NeoTCRseek improved the mean F1 score across the two neoantigen setups from 0.21 to 0.41.</p><p><strong>Conclusion: </strong>NeoTCRseek achieves high analytical sensitivity and accuracy in neoTCR clonotype identification and supports multi-antigen analysis, providing an integrated platform for neoTCR clonotype characterization and for tracking clinical T-cell dynamics in personalized cancer immunotherapy.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1674427"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13144021/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836533","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":"Case report: Persistent hypogammaglobulinemia following hematopoietic stem cell transplantation from a sibling donor with heterozygous RAG1 mutation.","authors":"Jing Wu, Huifang Wang, Weijie Chen, Zhiming Hong","doi":"10.3389/fimmu.2026.1798445","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1798445","url":null,"abstract":"<p><strong>Introduction: </strong>Hematopoietic stem cell transplantation (HSCT) is a curative treatment for pediatric hematologic and immunologic disorders, with successful immune reconstitution being critical for long-term survival. We report the unique case of persistent hypogammaglobulinemia following fully matched HSCT from a phenotypically normal sibling donor carrying a heterozygous <i>RAG1</i> gene mutation.</p><p><strong>Methods: </strong>A 13-year-old girl with EBV-associated NK/T-cell lymphoproliferative disorder underwent fully matched sibling HSCT from her mutation-carrying donor. Whole-exome sequencing confirmed the <i>RAG1</i> c.994C>T (p.Arg332*) mutation in both donor and recipient. Post-transplant monitoring included serial lymphocyte subset measurements and immunoglobulin level monitoring over a 5-year period.</p><p><strong>Results: </strong>Despite successful engraftment and quantitative T- and B-cell recovery, the patient developed persistent hypogammaglobulinemia. Serum IgG levels declined to below 4g/L at 4 months post-HSCT and remained persistently below 2g/L from 11 months onwards (with only one measurement of 2.57g/L during this period). IgA levels remained consistently below 0.2g/L, becoming undetectable by 11 months and remaining so. IgM levels dropped below the detection threshold at 2 months and demonstrated only partial recovery by 18 months (peak: 0.29g/L). The patient experienced recurrent respiratory infections, necessitating long-term immunoglobulin replacement therapy.</p><p><strong>Conclusions: </strong>This case demonstrates that heterozygous variants in genes critical for hematopoietic reconstitution (such as <i>RAG1</i> mutations) may still lead to significant immunodeficiency post-transplantation. Our findings strongly suggest that potential donors carrying such mutations require careful evaluation, with non-carrier donors being preferentially selected when available, especially in the context of HSCT.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1798445"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13147194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836774","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":"Deciphering the macrophage ferroptosis regulatory network: construction of an ulcerative colitis diagnostic model and investigation of the immune microenvironment based on single-cell and transcriptomic data.","authors":"Yifang Zhang, Zongchi Chen, Su Zhang, Yirong Chen, Chenhang Xie, Qinghua Xiao, Taiyong Fang","doi":"10.3389/fimmu.2026.1758082","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1758082","url":null,"abstract":"<p><strong>Background: </strong>Ulcerative colitis (UC) is a chronic inflammatory bowel disease manifested as persistent mucosal inflammation and immune dysregulation. As key regulators of intestinal immune homeostasis, macrophages are pivotal in the amplification of inflammation and tissue repair in UC. However, the molecular mechanisms associated with ferroptosis in macrophages remain unclear.</p><p><strong>Method: </strong>We integrated single-cell and bulk colonic transcriptomes to map ferroptosis-associated programs in UC macrophages, prioritized candidate regulators using network/ML frameworks, and performed targeted experimental validation.</p><p><strong>Results: </strong>We identified a ferroptosis-associated transcriptional program enriched in UC macrophages and derived a four-gene signature (HIF1A, S100A8, CYBB, GLS) linked to redox/iron stress. Among them, CYBB encodes NOX2 (the catalytic subunit of NADPH oxidase), and emerged as a key node associated with enhanced oxidative/iron stress and coordinated changes in ferroptosis-related markers in macrophages.</p><p><strong>Conclusion: </strong>This study systematically delineates the ferroptosis-associated transcriptional network in macrophages of UC, providing a systems-level framework linking macrophage redox/iron imbalance to ferroptosis vulnerability in UC and nominating CYBB-centered pathways for mechanistic interrogation and stratification-oriented biomarker development, thereby offering novel theoretical insights for immune metabolism mechanisms and targeted therapies in UC.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1758082"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836778","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":"Targeting cGAS-STING-macrophage axis: a novel therapeutic horizon for renal fibrosis.","authors":"Qi Wei, Kui Zhao, Fuyun Jia, Jing Zhou, Tianrui Liu, Shengwei Gao","doi":"10.3389/fimmu.2026.1809851","DOIUrl":"https://doi.org/10.3389/fimmu.2026.1809851","url":null,"abstract":"<p><p>Renal fibrosis, a pivotal pathological hallmark of chronic kidney disease (CKD), arises from persistent inflammatory responses and extracellular matrix (ECM) deposition. Emerging evidence indicates the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway has exerted a crucial influence on the progression of renal fibrosis. This pathway exacerbates the release of inflammatory factors and ECM deposition through reprograming the polarization state of macrophages, thereby driving renal fibrosis. This review delineates the regulatory role of the cGAS-STING signaling pathway in macrophage-related renal fibrosis and critically evaluates emerging innovative strategies targeting this pathway, including small molecule inhibitors, nanocarrier-based delivery systems, and gene editing technologies. However, current research still faces certain limitations, including the complexity of molecular mechanisms, differences in research results, and challenges in clinical translation. By synthesizing recent advances in cGAS-STING-mediated macrophage reprogramming for renal fibrosis intervention, this review aims to provide a foundation for precise therapeutic development.</p>","PeriodicalId":12622,"journal":{"name":"Frontiers in Immunology","volume":"17 ","pages":"1809851"},"PeriodicalIF":5.9,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836910","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}