Immunology最新文献

{"title":"Natural Killer Cell-Based Immunotherapy in HCC.","authors":"Linlin Che, Xueting Xie, Xiaoyu Yang, Shiguo Zhu, Yufu Zhou","doi":"10.1111/imm.70141","DOIUrl":"https://doi.org/10.1111/imm.70141","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) poses a formidable therapeutic challenge due to its high heterogeneity, frequent late-stage diagnosis, and chemoresistance. Natural killer (NK) cells are essential for immune surveillance, yet their quantity and function become significantly compromised during HCC progression, thereby promoting tumour immune escape. This review systematically outlines current NK cell-based immunotherapeutic strategies for HCC, including adoptive NK cell transfer, genetic engineering of NK cells, NK cell inhibitory receptor-targeted therapies, reprogramming of the immunosuppressive HCC microenvironment, cytokine-mediated enhancement of NK cell function, and traditional Chinese medicine-augmented NK cell cytotoxicity. Representing a promising immunotherapeutic paradigm, NK cell-based therapy is rapidly advancing from conventional cell infusion toward more precise modalities, including CAR-NK cells and multifunctional antibody engagers. However, the efficacy of these approaches is frequently curtailed by the immunosuppressive tumour microenvironment and tumour heterogeneity. Given the multifactorial nature of NK cell dysfunction, we highlight that rationally designed combination strategies-integrating genetic engineering, TME reprogramming, and checkpoint blockade-represent the most viable path toward durable clinical responses in HCC.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770363","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":"Dual Functions of Treg in the Mucosal Barrier and Lung Cancer Microenvironment and Prospects for Targeted Therapy.","authors":"Jiaming Cui, Jingru Han, Yang Dai, Shengqiang Li, Xinyu Wang, Ting Ge, Guixin He, Juyue Zhou, Li Yang, Yuanyuan Tian, Yingying Xie, Lefan Liu, Jinghui Du, Wentao Li, Li Liu, Jianchun Yu","doi":"10.1111/imm.70140","DOIUrl":"https://doi.org/10.1111/imm.70140","url":null,"abstract":"<p><p>Lung cancer remains one of the most common and deadly malignancies worldwide, representing a process intimately associated with dynamic changes in the tumour immune microenvironment. The pulmonary mucosal barrier, which serves as the first line of immune defence against pathogens and exogenous insults, not only restrains excessive inflammation by preserving local immune homeostasis but also actively participates in shaping the lung cancer microenvironment. Regulatory T cells (Tregs) are critical immunosuppressive cells that play a dual role in this context: they sustain immune tolerance by supporting mucosal barrier integrity and preventing autoimmunity, while concurrently mediating immunosuppression within the tumour niche to facilitate immune evasion and disease progression. Although recent years have seen considerable progress in elucidating the roles of the mucosal barrier and Tregs in lung cancer, their molecular regulatory networks and translational potential as therapeutic targets require further systematic investigation. This review synthesises current understanding of the interplay between the mucosal barrier and Tregs in the lung cancer immune microenvironment, with a focus on the functional balance between Treg-mediated immunosuppression and mucosal maintenance. Based on this, we propose an integrative conceptual framework-the \"mucosal-Treg-tumor immune axis\"-to reconcile the context-dependent duality of Tregs. It also evaluates current strategies and clinical prospects for targeting Tregs and associated signalling pathways in lung cancer immunotherapy, aiming to offer novel perspectives for therapeutic optimisation.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147770432","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":"Characterization of T-Cell Ubiquitination in Melanoma and Development of a Risk Signature Using Single-Cell and Bulk RNA-Seq.","authors":"Jianping Lu, Cheng Lin, Wei Gao, Jie Liu, Yucai Lin, Yu Chen, Jiani Xiong","doi":"10.1111/imm.70139","DOIUrl":"https://doi.org/10.1111/imm.70139","url":null,"abstract":"<p><p>Cutaneous melanoma (CM) is an aggressive cancer where early intervention is crucial, but the prognostic role and mechanisms of ubiquitination-related genes (URGs) in immune regulation remain unclear. This study aimed to develop a URG-based prognostic signature and explore its relationship with immune modulation in CM. We integrated single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data, identifying prognostic URGs through univariate and multivariate Cox regression. A six-gene signature (UBE2L6, SPSB1, PSMB9, PSMB10, RNF213 and ATXN3) was established and validated. The signature effectively stratified patients into high- and low-risk groups, with significant survival differences. Pathway analysis revealed immune-related processes, such as 'cytokine-cytokine receptor interaction' and 'antigen processing and presentation', enriched in the low-risk group. Immune cell infiltration analysis demonstrated significant differences in the abundance of 12 immune cell types between risk groups. Notably, PSMB9 expression was positively correlated with CD8⁺ T cell abundance (r = 0.64, p < 0.05). scRNA-seq analysis highlighted T cells as a key cell type, with all six prognostic genes showing dynamic expression changes during T cell differentiation. Our findings suggest that URGs influence CM prognosis by modulating the immune microenvironment, offering new insights for immunotherapeutic strategies.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728925","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":"Dual TLR7/8 Activation by Dihydroxyimidazoquinoline Adjuvant Orchestrates NF-κβ-iNOS-Driven Th1 Immunity and Durable Protection Against Leishmania donovani.","authors":"Shivani Thakur, Sandeep Kaur, Kushvinder Kumar, Deepak B Salunke, Sukhbir Kaur","doi":"10.1111/imm.70137","DOIUrl":"https://doi.org/10.1111/imm.70137","url":null,"abstract":"<p><p>Targeting Toll like receptors (TLRs) signalling represents a powerful approach to re-calibrate host immunity against intracellular pathogens. Among these, dual TLR7/8 agonists uniquely bridge innate and adaptive immune response through NF-κβ-associated cytokine programming and activation of innate effector pathways. Here we, identify and characterise a dihydroxyimidazoquinoline-based TLR7/8 agonist as a potent immunomodulatory adjuvant that enhances the efficacy of heat-killed Leishmania donovani antigen vaccine in BALB/c mice. Comparative immunisation with escalating adjuvant doses (10, 25 and 50 μg) demonstrated a robust, dose-dependent reduction in splenic parasite burden, accompanied by sustained elevation of Th1 cytokine (IFN-γ and TNF-α) and suppression of Th2-associated cytokine (IL-10 and IL-13) up to 16-week post-challenge. Enhanced iNOS and NF-κβ gene expression, together with elevated ROS and NO production, indicated activation of host effector pathways underlying parasite clearance. Flow cytometric analysis revealed persistent expansion of both CD4⁺ and CD8⁺ T cell subsets in the high-dose groups supporting durable adaptive immunity. The dual TLR7/8 activity of this compound mediated broad and sustained immunoregulatory signalling that surpassed resiquimod in magnitude and persistence. Collectively, this study delineated a mechanistic framework for TLR7/8 driven immunoregulation and establishes dihydroxyimidazoquinoline as a next-generation adjuvant for rational, host-directed vaccine design against intracellular pathogens such as L. donovani.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147672825","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":"Precision Glyco-Modulated GcMAF2.0 Targets CLEC10A to Bidirectionally Re-Wire Macrophage States: Cross-Species Evidence, Mechanistic Omics and Translational Horizons.","authors":"Evgeny Pokushalov, Dmitry Kudlay, Sergey Bogachev, Michael Johnson, Julia Snegireva, Richard Miller","doi":"10.1111/imm.70132","DOIUrl":"https://doi.org/10.1111/imm.70132","url":null,"abstract":"<p><p>Macrophages orchestrate inflammation, tissue repair and tumour surveillance, yet macrophage-targeted strategies such as CSF1R inhibition, CD47 blockade or TLR7/8 agonists have so far yielded only modest, context-restricted benefit. The C-type lectin CLEC10A (MGL/CD301) recognises a single terminal α-N-acetylgalactosamine (α-GalNAc) and couples this minimalist glycan cue to context-dependent inflammatory or reparative programmes, making it an attractive target for precision macrophage re-programming. This review synthesises mechanistic, pre-clinical and clinical data on Gc protein-derived macrophage-activating factor 2.0 (GcMAF2.0), a mono-α-GalNAc derivative of vitamin-D-binding protein that engages CLEC10A with high avidity. We summarise lessons from heterogeneous \"GcMAF1.0\" products, outline GMP workflows that yield EF-M1/EF-M2, and review CLEC10A-centred signalling and metabolic re-wiring, including SYK versus STAT6/PPARγ cascades and shifts in arginine, glucose and fatty-acid metabolism. Cross-species data from rodent inflammation models, human and canine myeloid cells, barrier-tissue and tumour models, and mesoscopic platforms indicate that α-GalNAc ligands and EF-M2 bias macrophage profiles and attenuate joint and barrier-tissue inflammation. A randomised double-blind placebo-controlled trial of EF-M2 in canine osteoarthritis links macrophage repolarisation to pain relief, gait restoration and serum ARG1/iNOS and IL-10/TNF-α shifts, providing disease-modifying proof of concept. We also review the small, uncontrolled human experience with analytically characterised GcMAF2.0 (≈120 patient-courses), noting favourable short-term tolerability but low certainty of benefit and a need for randomised, lot-traceable trials with mechanistic endpoints. Overall, we position the α-GalNAc-CLEC10A axis as a tunable handle on macrophage plasticity and outline the experimental and regulatory priorities needed to translate GcMAF2.0 into evidence-based immunotherapy.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147485693","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":"Inside Out: How Cellular Localisation Shapes cGAS Functions in Health and Disease.","authors":"Jiaqi Wu, Yingying Zhou, Bo Zeng, Yuan Wang, Chenhui Wang","doi":"10.1111/imm.70133","DOIUrl":"https://doi.org/10.1111/imm.70133","url":null,"abstract":"<p><p>The function of innate immune sensors is intricately shaped by their spatial distribution within cells. cGAS (cyclic GMP-AMP synthase), a key cytosolic DNA sensor, illustrates this principle through its unexpected localisation to diverse organelles-including the nucleus, micronuclei, mitochondria, and plasma membrane. In these compartments, cGAS assumes distinct regulatory states and executes specialised functions. For instance, chromatin-bound nuclear cGAS remains inactive under homeostasis but contributes to genome maintenance during genotoxic stress, whereas mitochondrial or micronuclear cGAS links damage signals to inflammation and cell death. This review synthesises recent advances in the spatial regulation of cGAS, focusing on mechanisms such as membrane interactions and post-translational modifications. We further reframe cGAS as a multifunctional regulator in infection, cancer, autoimmunity, and ageing, and introduce a unifying 'location code' framework. This framework proposes that the combined influence of PTMs, protein interactions, and membrane affinities dictates cGAS localisation, functional output, and pathological outcomes, thereby paving the way for spatially informed therapeutic interventions.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473653","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":"Blood Immunopathology of Tuberculosis Patients Disrupts Monocyte-Dependent T-Cell Activation and Cytokine Expression.","authors":"Joseph F Arthur, Hubert S Ahor, Monika M Vivekanandan, Difery Minadzi, Augustine Yeboah, Millicent Lamptey, Victoria A Ofori, Albert D Kegya, Rejoice Arthur, Linda A Amoakoa, Ernest Adankwah, Dorcas O Owusu, Mohammed K Abass, Fredrick Gyamfi Apraku, Nana K Ayisi-Boateng, Seth Adane, Salisu Zakaria, Ertan Mayatepek, Julia Seyfarth, Richard O Phillips, Marc Jacobsen","doi":"10.1111/imm.70131","DOIUrl":"https://doi.org/10.1111/imm.70131","url":null,"abstract":"<p><p>Pulmonary tuberculosis in humans is characterised by features of immunopathology, which influence both antimycobacterial therapy and the long-term prognosis. In the blood of tuberculosis patients, immunopathology manifests itself in reduced immune responses to mitogenic substances. Previous studies have demonstrated the influence of tuberculosis serum on T-cell and monocyte function, but the exact mechanisms remain unclear. Here, we performed a case/control study to analyse the influence of tuberculosis serum milieu changes on (i) T-cell stimulation (using Staphylococcal Enterotoxin B), (ii) monocyte stimulation (using the Toll-like receptor agonist Pam3CSK4), (iii) T-cell/monocyte interaction characterised by the response against the lectin phytohemagglutinin, by using a novel peripheral blood mononuclear cell in vitro assay. Cell-specific activation marker and cytokine expression were determined by multicolor flow cytometry. Staphylococcal Enterotoxin B mainly induced cytokine expression by T cells, while Pam3CSK4 stimulated monocytes to secrete distinct cytokine signatures. Phytohemagglutinin induced activation and cytokine expression in both T cells and monocytes. Notably, tuberculosis patient serum samples affected exclusively phytohemagglutinin stimulated T-cell responses and particularly activation marker as well as CD40L/IL-2 positive CD4⁺ T-cell subsets were decreased as compared to serum from healthy contacts. Neither Staphylococcal Enterotoxin B-mediated T-cell stimulation nor phytohemagglutinin or Pam3CSK4 induced monocyte cytokines (i.e., Interleukin-6, Interleukin-8, Tumour Necrosis Factor-α) were affected by the tuberculosis patients' serum samples. These results highlight the immunosuppressive influence of the tuberculosis serum milieu, which specifically reduced T-cell responses to phytohemagglutinin, probably through impaired function of the accessory monocytes required for stimulation.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377198","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":"SIRT6 Ameliorates Atherosclerosis by Inhibiting M1 Macrophage Polarisation Through Deacetylated-TLR4.","authors":"Jian Huang, Huiming Yi, Yanhui Wu, Wei Zhang, Xi Ai","doi":"10.1111/imm.70129","DOIUrl":"https://doi.org/10.1111/imm.70129","url":null,"abstract":"<p><p>Atherosclerosis serves as the fundamental pathological process underlying numerous cardiovascular disorders, and the change of macrophage polarisation is the key to regulate the inflammatory response of AS. SIRT6 plays a protective effect in AS, but whether it regulates macrophage polarisation in AS remains uncertain. We aimed to characterise the mechanistic role of SIRT6 in atherosclerosis development mediated by macrophage polarisation. ApoE^-/- mice were fed a Western diet to construct the AS mouse model, and LPS treatment was performed on RAW264.7 cells to induce an inflammation cell model. Quantitative real-time PCR was performed to measure the expression of SIRT6 and M1/M2 macrophage polarisation markers. Plaque size was evaluated by Oil red O staining. M1/M2 macrophage polarisation was evaluated by immunofluorescence staining. The underlying mechanism was determined by Western blot, immunoprecipitation (IP), and co-IP. Results suggested that SIRT6 was downregulated in the AS mouse model and LPS-induced macrophages. SIRT6 overexpression decreased plaque size and blood lipid levels in the AS mouse model and inhibited macrophages polarisation to the M1-like phenotype both in vivo and in vitro. Mechanically, SIRT6 overexpression downregulated the protein level of TLR4 by decreasing acetylation on TLR4. Moreover, TLR4 overexpression restored M1 macrophage polarisation in LPS-induced macrophages inhibited by SIRT6 overexpression. In conclusion, we demonstrated that SIRT6 attenuated AS by suppressing M1 macrophage polarisation through downregulating TLR4 by deacetylation. These results may provide a potential therapeutic target for targeted macrophage polarisation therapy for AS.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147377174","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":"Gut Microbiota-Induced CTLA4 Expression on CD8⁺ T Cells Impairs Antitumor Immunity and Promotes Colorectal Cancer Progression.","authors":"Meidie Cheng, Shuangcheng Zhi, Mengmeng Zheng, Sijin Zhang, Jun Hong","doi":"10.1111/imm.70128","DOIUrl":"https://doi.org/10.1111/imm.70128","url":null,"abstract":"<p><p>This study reveals a novel gut microbiota-CD8⁺ T cell axis driving immunosuppression in colorectal cancer. Analysis of 16S rRNA sequencing identified significant gut dysbiosis in CRC patients, with marked enrichment of Phocaeicola and Bacteroides. Single-cell transcriptomics uncovered substantial T cell depletion and elevated CTLA4⁺PD1⁺ immune cells within the tumour microenvironment. Critically, spatial transcriptomics demonstrated co-localization of CTLA4⁺CD8⁺ T cells with tumour cells, indicating direct immunosuppressive interactions. Functional validation confirmed CTLA4 overexpression impairs CD8⁺ T cell effector capacity, accelerating CRC cell proliferation and invasion. In vivo models demonstrated that faecal microbiota transplantation (FMT) promoted CTL activation, reduced Bacteroides abundance, decreased the formation of CD8⁺CTLA4⁺ T cells and ameliorated CRC symptoms. Additionally, CTLA4 knockdown inhibited tumour growth and metastasis. These findings establish a mechanistic pathway: gut dysbiosis induces chronic inflammation, triggering CTLA4 upregulation on CD8⁺ T cells to promote T cell exhaustion and tumour immune evasion. The study provides immunological evidence for targeting the microbiota-CTLA4 axis in CRC immunotherapy.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354840","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":"STING Drives Psoriatic Inflammation by Promoting Neutrophil Recruitment and Facilitating NETosis.","authors":"Haoyun Luo, Chenmin Hu, Tian Tian, Tian Qian, Xia Jiang, YongChao Dang, Bangtao Chen, Zhi Yang, Na Luo, Daojun Zhang, Fei Hao","doi":"10.1111/imm.70130","DOIUrl":"https://doi.org/10.1111/imm.70130","url":null,"abstract":"<p><p>Psoriasis is a chronic, immune-mediated inflammatory disorder in which neutrophils are central to pathogenesis. While recent studies have implicated the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway in psoriasis, its specific role in neutrophil-mediated inflammation remains unclear. To investigate neutrophil function in psoriasis, we integrated single-cell RNA-seq from human lesions with studies in IMQ-treated mouse models (wild-type, STING-/-, PADi4-/-) and HL-60 cells. We employed transcriptomic, cytometric and functional assays to assess neutrophil recruitment, cytokine secretion and neutrophil extracellular trap (NET) formation. Our study revealed significant upregulation of STING expression in both lesional and peripheral blood neutrophils of psoriasis patients. In the IMQ-induced mouse model, STING knockout markedly alleviated disease severity, reduced neutrophil infiltration and suppressed IL-1β release. Mechanistically, STING promoted neutrophil chemotactic migration via the IRF3/NF-κB axis while directly regulating the formation of NETs in neutrophils and the release of cytotoxic mediators. Besides, distinct mouse strains exhibited significant differences in STING pathway activation, indicating genetic heterogeneity in the immunoregulatory mechanisms underlying psoriasis. Collectively, the above findings indicated that STING signalling in neutrophil-mediated psoriatic inflammation not only regulates cell recruitment but also directly drives the terminal effector function of NETs production. Furthermore, strain-specific differences suggest that the regulation of this pathway in the disease context is complex and context-dependent, potentially influencing individualised therapeutic responses. Targeting the STING pathway could serve as a therapeutic strategy to simultaneously inhibit multiple pathogenic processes mediated by neutrophils.</p>","PeriodicalId":13508,"journal":{"name":"Immunology","volume":" ","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348242","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}