Immunological Investigations最新文献_第6页

Crosstalk Between Immunometabolic Pathways in Non-Small Cell Lung Cancer. 非小细胞肺癌免疫代谢途径间的串扰。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-09 DOI: 10.1080/08820139.2026.2698754

Riya Khilwani, Pooja Gulhane, Manasi Tukrul, Divya Rani, Gautam Kumar, Swati Goswami, Shailza Singh

{"title":"Crosstalk Between Immunometabolic Pathways in Non-Small Cell Lung Cancer.","authors":"Riya Khilwani, Pooja Gulhane, Manasi Tukrul, Divya Rani, Gautam Kumar, Swati Goswami, Shailza Singh","doi":"10.1080/08820139.2026.2698754","DOIUrl":"https://doi.org/10.1080/08820139.2026.2698754","url":null,"abstract":"Background: Immunometabolic reprogramming has emerged as a key regulator of both innate and adaptive immune responses. In NSCLC, immunometabolism not only sustains tumor growth but also enables immune evasion through altering the immune cell behavior within the tumor microenvironment. Despite multiple signaling pathways having been implicated in the process, the integration of inflammatory cytokines and metabolic signaling underlying autophagy dysregulation in NSCLC remains unexplored.Objective: From a cellular perspective, the review summarizes the immunometabolic and regulatory functions of IL-6 and IL-17 in inflammaphagy and their integration into immunometabolic networks. The conserved contributions of key regulatory pathways, including BMP, DUSP, FOXO, SPROUTY, and STING, in shaping immune cell metabolism and tumor progression were also underscored.Methods: A narrative review of recent literature was performed focusing on integrating findings from experimental and clinical studies to construct a unified framework defining cytokine interactions, immune metabolism, and tumor progression.Results: IL-6 and IL-17 are critical regulators for metabolically adapting tumor cells while influencing macrophages, T-cells, neutrophils, and other immune subsets towards attaining a metabolic shift. Additionally, conserved trajectories of BMP, DUSP, FOXO, SPROUTY, and STING modulate metabolic homeostasis for tumor development, highlighting their crosstalk between inflammatory and metabolic networks.Conclusion: Advances in understanding the interconnected role of inflammatory cytokines, autophagy, and metabolism may identify novel therapeutic targets and improve the effectiveness of immunotherapy towards achieving the goal of precision oncology.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-40"},"PeriodicalIF":2.3,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Emerging Role of Tumor-Associated Neutrophils in Modulating Immune Checkpoint Inhibitor Response and Therapeutic Strategies. 肿瘤相关中性粒细胞在调节免疫检查点抑制剂反应和治疗策略中的新作用。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-03 DOI: 10.1080/08820139.2026.2689677

Duanting Liu, Yunru Gu, Xiaoxiang Guan

{"title":"The Emerging Role of Tumor-Associated Neutrophils in Modulating Immune Checkpoint Inhibitor Response and Therapeutic Strategies.","authors":"Duanting Liu, Yunru Gu, Xiaoxiang Guan","doi":"10.1080/08820139.2026.2689677","DOIUrl":"https://doi.org/10.1080/08820139.2026.2689677","url":null,"abstract":"Background: The tumor microenvironment (TME) is a highly complex and dynamic ecosystem composed of diverse immune cell populations. Among them, tumor-associated neutrophils (TANs) have gained increasing attention due to their dual roles in tumor progression and immunomodulation. Although neutrophils are traditionally recognized as key effector cells of the innate immune system against microbial infection, accumulating evidence highlights their functional plasticity in cancer.Methods: This review systematically summarizes and analyzes published literature focusing on TAN biology, immune regulatory mechanisms, and their impact on immune checkpoint inhibitor (ICI) therapy responses.Results: Current evidence indicates that TANs contribute to tumor initiation and progression through multiple molecular and cellular pathways. They actively participate in immune evasion within the TME and can modulate the efficacy of ICIs. Mechanistically, TANs influence anti-tumor immunity through diverse signaling networks and cellular interactions that reshape the immune landscape of tumors.Conclusion: Targeting TAN-associated pathways represents a promising strategy to improve ICI therapeutic efficacy. A deeper understanding of TAN-mediated immune regulation provides a useful framework for developing novel cancer immunotherapy approaches.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-29"},"PeriodicalIF":2.3,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148381979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

UBE2I Alleviates Pyroptosis in Coronary Heart Disease by Promoting the SUMOylation and Degradation of NLRP3. UBE2I通过促进NLRP3的sumo化和降解来减轻冠心病患者的焦亡。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-04-03 DOI: 10.1080/08820139.2026.2651753

Sheng-Kai Ding

{"title":"UBE2I Alleviates Pyroptosis in Coronary Heart Disease by Promoting the SUMOylation and Degradation of NLRP3.","authors":"Sheng-Kai Ding","doi":"10.1080/08820139.2026.2651753","DOIUrl":"10.1080/08820139.2026.2651753","url":null,"abstract":"Objective: Coronary heart disease (CHD), a major cardiovascular disorder, involves myocardial injury, inflammation, and fibrosis. NLRP3 inflammasome-driven pyroptosis plays a critical role in CHD progression. Although the ubiquitin-conjugating enzyme E2I (UBE2I) regulates protein SUMOylation, its function in CHD remains poorly understood. This study explores the expression and role of UBE2I in CHD, specifically examining its potential to mitigate myocardial injury and fibrosis via regulation of NLRP3 SUMOylation and pyroptosis.Methods: An in vivo CHD model was established using APOE-/- mice fed a high-fat diet, followed by lentivirus-mediated UBE2I overexpression. In vitro, ox-LDL-induced H9C2 cardiomyocytes were transfected with UBE2I overexpression or knockdown plasmids. Cardiac function, fibrosis, inflammatory cytokines, and pyroptosis were assessed via echocardiography, Masson staining, ELISA, flow cytometry, qPCR, and immunoblotting. Protein interactions and SUMOylation were evaluated using co-immunoprecipitation and site-directed mutagenesis.Results: UBE2I expression was significantly downregulated in CHD mice and ox-LDL-induced H9C2 cells. Overexpression of UBE2I improved cardiac function, reduced myocardial injury markers, attenuated fibrosis, and decreased levels of pro-inflammatory cytokines. It also suppressed NLRP3-mediated pyroptosis. Mechanistically, UBE2I promoted SUMOylation of NLRP3 at lysine 202, leading to its destabilization and degradation. Overexpression of NLRP3 reversed the protective effects of UBE2I in vitro.Conclusions: This study provided a new perspective for the treatment of CHD, that is, UBE2I accelerated the degradation of NLRP3 through the SUMOylation pathway, thereby exerting an anti-pyroptosis effect. Therefore, UBE2I was a promising therapeutic target for CHD.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"908-927"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147608694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of Tumour-Infiltrating Lymphocytes in the Immune Microenvironment of Lymphoma and Their Immunotherapeutic Potential. 肿瘤浸润淋巴细胞在淋巴瘤免疫微环境中的作用及其免疫治疗潜力。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-05-11 DOI: 10.1080/08820139.2026.2645948

Dezhi Yu, Kaiyun Guo, Chao Wang, Yao Zhang, Wu Jian, Ming Lei, Yuting Lei, Chunlian Zhao

{"title":"The Role of Tumour-Infiltrating Lymphocytes in the Immune Microenvironment of Lymphoma and Their Immunotherapeutic Potential.","authors":"Dezhi Yu, Kaiyun Guo, Chao Wang, Yao Zhang, Wu Jian, Ming Lei, Yuting Lei, Chunlian Zhao","doi":"10.1080/08820139.2026.2645948","DOIUrl":"10.1080/08820139.2026.2645948","url":null,"abstract":"Background: Tumour-infiltrating lymphocytes (TILs), including CD8+ T cells, CD4+ T cells, B cells and natural killer cells, play a key role in anti-tumour immune responses and modulate tumour immune escape via crosstalk with immunosuppressive factors in the tumour microenvironment. Despite inherent anti-tumour activity, TIL function is largely constrained by immune escape and cellular exhaustion. TILs also synergise with PD-1/PD-L1 and CTLA-4 to regulate the magnitude and persistence of anti-tumour immunity, and have emerged as valuable biomarkers for evaluating immunotherapeutic efficacy in lymphoma.Methods: This review systematically summarises recent published literature regarding the biological function, immune regulatory mechanisms and clinical research progress of TILs in lymphoma.Results: TILs exhibit promising potential in lymphoma immunotherapy, whereas TIL-based strategies remain challenged by complex cell preparation, unstable therapeutic efficacy and drug resistance. Further research is required to clarify TIL heterogeneity, characterise diverse immune escape mechanisms, and optimise clinical culture protocols.Conclusions: This review clarifies the pivotal role of TILs in the lymphoma immune microenvironment and their immunotherapeutic value. Optimising TIL culture conditions combined with gene editing and bioengineering will improve therapeutic efficacy and clinical applicability, offering novel insights for clinical treatment of lymphoma.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"928-947"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Causal Role of Circulating Inflammatory Cytokines in Brain Tumors: Insights from Genetic Epidemiology. 循环炎性细胞因子在脑肿瘤中的因果作用：来自遗传流行病学的见解。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-03-23 DOI: 10.1080/08820139.2026.2647055

Teng Qi, Lingjun Yao, Zheyu Wen, Xiaorui Zhou, Hanqing Zhao, Jiazhen He, Jing Hu

{"title":"The Causal Role of Circulating Inflammatory Cytokines in Brain Tumors: Insights from Genetic Epidemiology.","authors":"Teng Qi, Lingjun Yao, Zheyu Wen, Xiaorui Zhou, Hanqing Zhao, Jiazhen He, Jing Hu","doi":"10.1080/08820139.2026.2647055","DOIUrl":"10.1080/08820139.2026.2647055","url":null,"abstract":"Background: Previous studies indicate associations between inflammatory cytokines and glioma, meningioma, and astrocytoma.Methods: We conducted two-sample Mendelian randomization with genetic data for tumors from FinnGen R10 and cytokine data from GWAS. Primary analysis used inverse variance weighting, supplemented by sensitivity analyses including weighted median, simple mode, weighted mode, and MR-Egger.Results: For glioma, TNF-related apoptosis-inducing ligand (TRAIL) was a risk factor, while Fibroblast growth factor 21 (FGF21) was protective. For meningioma, Axin-1 and Matrix metalloproteinase-1 were risk factors, whereas Fms-related tyrosine kinase 3 ligand was protective. For astrocytoma, risk factors included Eotaxin, Macrophage colony-stimulating factor 1, and Interleukin-8; protective factors were T-cell surface glycoprotein CD5 and Tumor necrosis factor ligand superfamily member 12.Conclusions: This Mendelian randomization study identified specific inflammatory cytokines associated with these tumors, providing direction for future mechanistic research.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"873-888"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147498577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunometabolic Dysregulation in Psoriasis: Mechanisms Driving Inflammation and Emerging Therapeutic Targets. 银屑病的免疫代谢失调：驱动炎症的机制和新出现的治疗靶点。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-03-16 DOI: 10.1080/08820139.2026.2645963

Aditya Jaswal, Aman Kumar, Preeti Patel, Balak Das Kurmi

{"title":"Immunometabolic Dysregulation in Psoriasis: Mechanisms Driving Inflammation and Emerging Therapeutic Targets.","authors":"Aditya Jaswal, Aman Kumar, Preeti Patel, Balak Das Kurmi","doi":"10.1080/08820139.2026.2645963","DOIUrl":"10.1080/08820139.2026.2645963","url":null,"abstract":"Background: Psoriasis is increasingly recognized as a systemic immuno-metabolic disorder in which chronic inflammation interacts with alterations in cellular energy metabolism.Objective: To summarize current evidence on immunometabolic dysregulation in psoriasis and highlight emerging metabolic-targeted therapeutic strategies.Methods: A narrative review of recent literature examining metabolic pathways, immune responses, and therapeutic interventions involved in psoriasis pathogenesis was conducted.Results: Psoriatic keratinocytes, T cells, dendritic cells, and macrophages undergo significant metabolic reprogramming characterized by increased glycolysis, altered lipid metabolism, mitochondrial dysfunction, and excessive reactive oxygen species production. These metabolic disturbances contribute to keratinocyte hyperproliferation and sustain Th17-driven inflammation, linking skin pathology with systemic comorbidities such as obesity, insulin resistance, dyslipidaemia, and endothelial dysfunction. Key nutrient-sensing regulators, including mechanistic target of rapamycin (mTOR), AMP-activated protein kinase (AMPK), hypoxia-inducible factor-1α (HIF-1α), sirtuin-1 (SIRT1), and PGC-1α, integrate metabolic status with inflammatory signaling. Additionally, adipokine imbalance and metabolic stress promote chronic metaflammation.Conclusion: Targeting immunometabolic pathways through glycolysis inhibitors, AMPK activators, mTOR modulators, mitochondrial-targeted antioxidants, and lipid-regulating agents may restore metabolic homeostasis and reduce inflammation. Advances in multi-omics approaches may further facilitate biomarker discovery and precision-based therapeutic strategies in psoriasis management.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"948-974"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic Risk Factors in Autoimmune Thyroid Diseases: An Umbrella Review of Meta-Analyses and Evidence Credibility. 自身免疫性甲状腺疾病的遗传危险因素：荟萃分析和证据可信度综述

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-04-20 DOI: 10.1080/08820139.2026.2658603

Anu Shibi Anilkumar, Nithya Ajay, Ramakrishnan Veerabathiran

{"title":"Genetic Risk Factors in Autoimmune Thyroid Diseases: An Umbrella Review of Meta-Analyses and Evidence Credibility.","authors":"Anu Shibi Anilkumar, Nithya Ajay, Ramakrishnan Veerabathiran","doi":"10.1080/08820139.2026.2658603","DOIUrl":"10.1080/08820139.2026.2658603","url":null,"abstract":"Background Autoimmune thyroid diseases (AITDs) include Graves' disease and Hashimoto's thyroiditis, embodying a group of complex immune-regulated disorders characterized by a high degree of genetic predisposition. The results from various meta-analyses on AITD-related polymorphisms are still conflicting due to heterogeneity, population-specific effects, and the presence of poor-quality studies.MethodsThis umbrella review aims to merge and critically assess the findings from published meta-analyses to locate the valid genetic risk factors for AITDs. Meta-analyses published between 2005 and 2025 were accessed from databases and estimated using standard evidence-grading frameworks, including AMSTAR-2, GRADE, and the Venice criteria. Evidence was interpreted by integrating pooled effect estimates, heterogeneity, total sample sizes, and subgroup consistency.Results Among the assessed loci, TSHR polymorphisms yielded consistent associations with GD, supported by relatively large sample sizes, low heterogeneity, extensive study volume, and medium-to-high evidence certainty across study groups. CTLA-4 and PTPN22 variants showed heterogeneity-moderated associations with possible ethnicity-dependent effects. In contrast, FOXP3, cytokine genes, VDR, MTHFR, and TG polymorphisms showed unstable or low-certainty evidence, primarily due to high heterogeneity and fewer studies.Conclusion Thus, this study provides a hierarchical framework for interpreting genetic susceptibility in AITDs, helping to prioritize robust loci for functional validation and translational research.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1054-1103"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147722160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoding the Skin Micro-Immune Milieu, Homeostasis, and Keratinocyte Trafficking in Psoriatic Disease. 解读银屑病的皮肤微免疫环境、体内平衡和角化细胞运输。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-04-08 DOI: 10.1080/08820139.2026.2651752

Ishu Garg, Neelam Singh, Shivani Rawat, Tushar Negi, Urmi Chaurasia, Punnet Gupta

{"title":"Decoding the Skin Micro-Immune Milieu, Homeostasis, and Keratinocyte Trafficking in Psoriatic Disease.","authors":"Ishu Garg, Neelam Singh, Shivani Rawat, Tushar Negi, Urmi Chaurasia, Punnet Gupta","doi":"10.1080/08820139.2026.2651752","DOIUrl":"10.1080/08820139.2026.2651752","url":null,"abstract":"Introduction: The skin, acting as a complex interface between the immune system and microbiome, maintains balance through coordinated interactions among the epidermal barrier, microbiome, and immune responses. Psoriasis, a chronic autoimmune and inflammatory disorder, disrupts this balance by altering keratinocyte growth, immune signaling, and microbial diversity.Results and discussion: The psoriatic environment exhibits dysbiosis, with reduced α-diversity and increased β-diversity, thereby worsening lesions. Beneficial microbes like Staphylococcus epidermidis provide protection, while opportunistic pathogens such as Staphylococcus aureus, Streptococcus pyogenes, Malassezia, Candida albicans, and HPV can trigger psoriatic outbreaks. Keratinocytes, essential to disease development and progression, interact actively with immune cells, fibroblasts, and Langerhans cells through cytokines, chemokines, and extracellular vesicles, influencing cell movement and inflammation. Changes in pathways like GLUT-1-mediated glucose metabolism and PI3K/Akt/mTOR signaling promote epidermal overgrowth, new blood vessel formation, and immune imbalance. Oxidative stress and mitochondrial dysfunction also weaken skin homeostasis. The skin's lymphoid tissue (SALT) and inducible SALT are crucial for immune surveillance and autoimmunity but become hyperactive in psoriasis.Conclusion: Understanding the complex network linking the skin microbiome, immune system, and keratinocyte behavior is essential for developing advanced treatments. Combining immunology, molecular biology, and drug delivery science, using molecular docking, in-silico modeling, and nanotherapy, offers promising options for targeted psoriasis therapy.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"998-1028"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147633399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The STING-Inflammasome Axis: Coordinated Immune Regulation and Therapeutic Potential Across Diverse Diseases. sting -炎性体轴：不同疾病的协调免疫调节和治疗潜力。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 Epub Date: 2026-05-06 DOI: 10.1080/08820139.2026.2659339

Yu Chen, BingXiao Zhang, ChenGuang Wang, WenFeng Gou, YiLiang Li, WenBin Hou, FeiFei Xu

{"title":"The STING-Inflammasome Axis: Coordinated Immune Regulation and Therapeutic Potential Across Diverse Diseases.","authors":"Yu Chen, BingXiao Zhang, ChenGuang Wang, WenFeng Gou, YiLiang Li, WenBin Hou, FeiFei Xu","doi":"10.1080/08820139.2026.2659339","DOIUrl":"10.1080/08820139.2026.2659339","url":null,"abstract":"Introduction: The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway and inflammasomes were long regarded as distinct innate immune modules that respond to different classes of danger signals. However, accumulating evidence now reveals extensive, bidirectional crosstalk between these pathways, forming an integrated regulatory network that critically shapes the magnitude, quality, and outcome of immune responses. The balance of this network determines whether the host mounts effective pathogen control and tumor immunosurveillance, or instead succumbs to excessive inflammation, tissue injury, or autoimmune pathology.Results and discussion: In this review, we synthesize current mechanistic understanding of STING-inflammasome interactions, highlighting how shared upstream triggers - particularly cytosolic DNA - coordinate the activation, amplification, or restraint of these pathways. We further examine how this axis exerts context-dependent, dualistic functions across diverse disease settings, including cancer, autoimmunity, neurodegeneration, chronic infection, and aging. From a pharmacological perspective, we discuss emerging therapeutic strategies aimed at modulating key regulatory nodes within this signaling network, ranging from STING agonists for cancer immunotherapy to selective STING or the NLR family pyrin domain-containing 3 (NLRP3) inhibitors for autoimmune and inflammatory diseases.Conclusion: Together, these insights provide a conceptual and translational foundation for the rational development of next-generation immunomodulatory agents targeting the STING-inflammasome axis.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1104-1125"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immune Reconstitution After Hematopoietic Stem Cell Transplantation: Cellular Dynamics, Clinical Determinants, and Emerging Therapeutic Strategies. 造血干细胞移植后的免疫重建：细胞动力学、临床决定因素和新兴治疗策略。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-01 DOI: 10.1080/08820139.2026.2696004

Eida Elmansorry

{"title":"Immune Reconstitution After Hematopoietic Stem Cell Transplantation: Cellular Dynamics, Clinical Determinants, and Emerging Therapeutic Strategies.","authors":"Eida Elmansorry","doi":"10.1080/08820139.2026.2696004","DOIUrl":"https://doi.org/10.1080/08820139.2026.2696004","url":null,"abstract":"Background: Immune reconstitution following HSCT is a complex process that strongly determines post-transplant outcomes. Delayed or impaired immune recovery increases susceptibility to opportunistic infections, viral reactivation, graft-versus-host disease, relapse, and transplant-related morbidity and mortality.Objective: This review summarizes current evidence on the kinetics, functional recovery, and clinical significance of innate and adaptive immune reconstitution after HSCT.Methods: A narrative review of recent literature was performed focusing on immune cell reconstitution dynamics and influencing clinical and biological factors.Results: Innate immunity (neutrophils, NK cells) recovers early, providing initial defense. Adaptive immunity is delayed, driven by thymic output and peripheral T- and B-cell expansion. Regulatory T cells and γδ T cells support tolerance and graft-versus-leukemia effects. Recovery is influenced by age, conditioning, graft source, GVHD, infections, and microbiome. Numerical recovery may not equal functional immune competence.Conclusion: Advances in immune profiling, biomarkers, and systems immunology, along with adoptive cellular therapy and microbiome-based interventions, may enable personalized strategies to improve immune reconstitution and long-term outcomes.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-31"},"PeriodicalIF":2.3,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0