Immunological Investigations最新文献_第5页

Interferon-Associated Antiviral Programs Define LAG-3+ Exhaustion-Like CD8+ T-Cell Remodeling in Influenza a Virus Infection: An Integrative Single-Cell and Multi-Cohort Analysis. 干扰素相关抗病毒程序定义了甲型流感病毒感染中LAG-3+耗尽样CD8+ t细胞重塑：一项综合单细胞和多队列分析

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-30 DOI: 10.1080/08820139.2026.2712508

Yecheng Zhou, Jianing Wang, Jingyan Xu, Yun Pan, Hanjin Zou, Jiaxiong Tan

{"title":"Interferon-Associated Antiviral Programs Define LAG-3+ Exhaustion-Like CD8+ T-Cell Remodeling in Influenza a Virus Infection: An Integrative Single-Cell and Multi-Cohort Analysis.","authors":"Yecheng Zhou, Jianing Wang, Jingyan Xu, Yun Pan, Hanjin Zou, Jiaxiong Tan","doi":"10.1080/08820139.2026.2712508","DOIUrl":"https://doi.org/10.1080/08820139.2026.2712508","url":null,"abstract":"Background: Influenza A virus (IAV) infection induces complex antiviral immune responses, yet how innate sensing, host genetic susceptibility, and adaptive immune dysfunction converge remains incompletely understood. This study investigated peripheral immune remodeling during IAV infection, focusing on LAG-3-expressing CD8+ T cells and their transcriptional and genetic signatures.Methods: Single-cell and bulk transcriptomics, genetic analyses, Mendelian randomization, network modeling, and machine learning were integrated. Flow cytometry was used to validate LAG-3 expression and CD8+ T-cell dysfunction in healthy controls and children with IAV infection.Results: IAV infection caused marked immune remodeling and expansion of LAG-3+ exhaustion-like CD8+ T cells spanning naïve, effector, and exhaustion-associated states. Interferon-stimulated genes dominated differential expression, co-expression modules, and pathway enrichment. Ten influenza-exhaustion signature genes were identified, with Mendelian randomization prioritizing IFI44, IFIT3, MX2, ZBP1, IFIT1, and HES4 as genetically associated with IAV susceptibility. Gene-based classifiers achieved AUCs up to 0.886 across three independent cohorts. Flow cytometry confirmed increased LAG-3 expression and reduced CD107a activity in pediatric IAV infection.Conclusions: IAV infection is characterized by an interferon-dominated program and expansion of dysfunctional LAG-3+ CD8+ T cells, highlighting candidate biomarkers for immune remodeling.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-30"},"PeriodicalIF":2.3,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630323","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 Microglial NLRP3 Inflammasome in Multiple Sclerosis: Bridging Innate Immunity, Chronic Inflammation, and IFN-β Response. 多发性硬化症中的小胶质NLRP3炎性小体：连接先天免疫、慢性炎症和IFN-β反应。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-27 DOI: 10.1080/08820139.2026.2702083

Prathyusha Koyya, Hemasundar Alavilli, Santhi Latha Pandrangi, Ram Kumar Manthari

{"title":"The Microglial NLRP3 Inflammasome in Multiple Sclerosis: Bridging Innate Immunity, Chronic Inflammation, and IFN-β Response.","authors":"Prathyusha Koyya, Hemasundar Alavilli, Santhi Latha Pandrangi, Ram Kumar Manthari","doi":"10.1080/08820139.2026.2702083","DOIUrl":"https://doi.org/10.1080/08820139.2026.2702083","url":null,"abstract":"Background: Multiple sclerosis (MS) is a chronic neurodegenerative and demyelinating disease that is marked by chronic inflammation of the central nervous system (CNS). Although interferon-β (IFN-β) remains one of the pillars of treatment for relapsing-remitting MS (RRMS), inconsistencies in the responses of patients signify the necessity to comprehend the immunopathological processes.Objectives: The NLRP3 (NOD-like receptor family pyrin domain-containing 3) inflammasome, an intracellular signaling platform controlling the activation of caspase-1 and the maturation of interleukin-1β (IL-1β) and interleukin-18 (IL-18) has been of considerable interest among emerging molecular actors. Microglia, the native CNS macrophage, are the center stage of tissue damage and repair.Results: Demyelination and axonal degeneration in neuroinflammation are linked to the role of aberrant activity of the microglial NLRP3 inflammasome. In addition, it is also suggested that an inhibition of inflammasome by IFN-β can be observed in a mechanistic interaction between NLRP3 signaling and response to treatment.Conclusion: In this literature review, the presented data summarize the existing information about the contribution of NLRP3 to the pathogenesis of MS disease, microglial activation, and IFN-β regulation, and how this pathway can be applied to shape personalized treatment approaches.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-15"},"PeriodicalIF":2.3,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148591358","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

Statement of Retraction: Short-Chain Fatty Acids Regulate Cytokines and Th17/Treg Cells in Human Peripheral Blood Mononuclear Cells in vitro. 撤回声明：短链脂肪酸在体外调节人外周血单核细胞中的细胞因子和Th17/Treg细胞。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-22 DOI: 10.1080/08820139.2026.2706222

引用次数: 0

The ATG14-SIRT1 Axis Modulates NF-Κb Pathway Activation and Inflammatory Responses in Acute Lung Injury. ATG14-SIRT1轴调节NF-Κb通路激活和急性肺损伤的炎症反应。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-22 DOI: 10.1080/08820139.2026.2697466

Yali Wang, Zilong Liu, Haiying Ji, Lei Zhu

{"title":"The ATG14-SIRT1 Axis Modulates NF-Κb Pathway Activation and Inflammatory Responses in Acute Lung Injury.","authors":"Yali Wang, Zilong Liu, Haiying Ji, Lei Zhu","doi":"10.1080/08820139.2026.2697466","DOIUrl":"https://doi.org/10.1080/08820139.2026.2697466","url":null,"abstract":"Background: Acute lung injury (ALI) is characterized by dysregulated inflammation and tissue damage. Autophagy-related gene 14 (ATG14) is a key autophagy regulator, but its role in ALI remains incompletely understood.Methods: LPS-induced ALI was investigated in mice and lung epithelial cells. Autophagy, ATG14 acetylation, NF-κB pathway activation, and cytokine production were evaluated by histology, western blotting, immunoprecipitation, ELISA, electron microscopy, mass spectrometry, and molecular docking. ATG14 knockdown/overexpression and SIRT1 overexpression were used to explore mechanisms.Results: LPS induced excessive autophagy, increased ATG14 expression and acetylation in lung tissue, reduced epithelial ATG14 levels through TLR4-dependent proteasomal degradation in vitro, reduced SIRT1 levels, and enhanced NF-κB pathway activity. SIRT1 interacted with ATG14 and suppressed its acetylation. Peptide docking supported the structural feasibility of SIRT1 recognition of ATG14 regions containing K78 and K178, with the K178-containing region showing a more compatible orientation near the SIRT1 catalytic surface. ATG14 inhibition or SIRT1 restoration reduced NF-κB pathway activity, cytokine production, and lung inflammation in vitro and in vivo.Conclusion: The ATG14-SIRT1 axis modulates autophagy-inflammation crosstalk in ALI and may represent a potential therapeutic target.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-29"},"PeriodicalIF":2.3,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561882","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

Adiponectin Signaling as an Immunometabolic Regulator in COVID-19: Mechanistic Insights and Therapeutic Potential. 脂联素信号作为COVID-19免疫代谢调节因子：机制见解和治疗潜力。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-21 DOI: 10.1080/08820139.2026.2704902

Ali Abdullah Alqarni, Hayder M Al-Kuraishy, Mohammed Alqarni, Duaa Eliwa, Ali I Al-Gareeb, Mostafa M Bahaa, Gaber El-Saber Batiha

{"title":"Adiponectin Signaling as an Immunometabolic Regulator in COVID-19: Mechanistic Insights and Therapeutic Potential.","authors":"Ali Abdullah Alqarni, Hayder M Al-Kuraishy, Mohammed Alqarni, Duaa Eliwa, Ali I Al-Gareeb, Mostafa M Bahaa, Gaber El-Saber Batiha","doi":"10.1080/08820139.2026.2704902","DOIUrl":"https://doi.org/10.1080/08820139.2026.2704902","url":null,"abstract":"Background: Adiponectin is a pleiotropic adipocytokine with anti-inflammatory, antioxidant, and insulin-sensitizing functions. Its regulatory role in glucose and lipid metabolism, endothelial homeostasis, and immune responses positions it as a key determinant of immunometabolic resilience. Dysregulated adiponectin signaling has been increasingly implicated in adverse COVID-19 outcomes, particularly among individuals with metabolic comorbidities.Objective: To synthesize mechanistic, preclinical, and translational evidence on adiponectin signaling in COVID-19 and evaluate its potential as a therapeutic and lifestyle-modulated target.Methods: A critical review of published literature on adiponectin biology, AdipoR1/R2 receptor signaling, AMPK and PPAR-α pathways, cytokine regulation, oxidative stress, and infection-induced metabolic reprogramming was conducted.Results: COVID-19 is consistently associated with reduced circulating adiponectin, with the greatest declines observed in obesity, diabetes, and metabolic syndrome. Mechanistic and animal studies show that adiponectin activation attenuates hyperinflammation, oxidative stress, endothelial dysfunction, and multi-organ injury. These effects are mediated through AMPK activation, PPAR-α modulation, NF-κB suppression, and restoration of metabolic-immune balance.Conclusions: Adiponectin signaling represents a promising therapeutic target for mitigating COVID-19 severity, especially in metabolically vulnerable populations. Pharmacological agonists and lifestyle interventions that enhance adiponectin pathways warrant further translational investigation.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-24"},"PeriodicalIF":2.3,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548770","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

Breaking and Making Tolerance: The PD-1/PD-L1 Axis in Lupus Nephritis. 破造耐受性：狼疮性肾炎患者PD-1/PD-L1轴。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-20 DOI: 10.1080/08820139.2026.2699369

Yachao Li, Xinyi Fang, Xiang Gao, Chi Liu

{"title":"Breaking and Making Tolerance: The PD-1/PD-L1 Axis in Lupus Nephritis.","authors":"Yachao Li, Xinyi Fang, Xiang Gao, Chi Liu","doi":"10.1080/08820139.2026.2699369","DOIUrl":"https://doi.org/10.1080/08820139.2026.2699369","url":null,"abstract":"Background: The PD-1/PD-L1 axis is a key immune checkpoint that maintains peripheral tolerance by restraining T-cell activation. In lupus nephritis (LN), this pathway has long been viewed as protective, based on Pdcd1-deficient mice developing lupus-like nephritis and PD-L1 fusion protein efficacy in mouse models. However, recent clinical findings reveal a paradox: PD-1⁺ T cells - especially CD8⁺ and CD4⁺ subsets - are greatly expanded in blood and kidneys of LN patients, correlating with disease activity, proteinuria, and renal decline.Objective: To reconcile the protective and pathogenic roles of PD-1/PD-L1 signaling and propose a unifying \"signal balance model\" for precision immunomodulation.Findings: These PD-1⁺ cells are not exhausted but exhibit an activated, clonally expanded effector phenotype (granzyme B, perforin, IFN-γ) that drives tissue injury, while PD-1⁺ Tph and Tfh cells promote autoantibody production. The biphasic nature of PD-1/PD-L1 signaling arises from T-cell subset heterogeneity, inflammatory cytokines (IL-12, IFN-α) that override inhibition, costimulatory signals, and reverse signaling through PD-L1 on renal parenchymal cells.Conclusions: We propose that the net outcome - protection versus pathogenesis - depends on the relative weights of these four determinants, further influenced by genetic background (e.g., PDCD1 polymorphisms). PD-1 agonism (rosnilimab, PD-L1-Fc, nanoparticle delivery) offers promise, but the pathogenic activity of PD-1⁺ effector T cells argues against a uniform approach. Our framework provides a basis for patient stratification, biomarker development, and combination strategies, ultimately guiding a shift from broad immunosuppression to tailored therapy in LN and informing future translational research.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148520293","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

Long Non-Coding RNAs in Natural Killer Cell Biology: Insights into Immune Regulation and Cancer. 自然杀伤细胞生物学中的长链非编码rna：对免疫调节和癌症的见解。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-16 DOI: 10.1080/08820139.2026.2702577

Sarah Abouhegaziah, Carsten Watzl, Mona Rady

{"title":"Long Non-Coding RNAs in Natural Killer Cell Biology: Insights into Immune Regulation and Cancer.","authors":"Sarah Abouhegaziah, Carsten Watzl, Mona Rady","doi":"10.1080/08820139.2026.2702577","DOIUrl":"https://doi.org/10.1080/08820139.2026.2702577","url":null,"abstract":"Background: Natural Killer (NK) cells are essential innate immune effectors that provide constant surveillance by inducing apoptosis in infected and malignant cells primarily through degranulation. Long non-coding RNAs (lncRNAs) are regulatory transcripts (>200 nucleotides) that modulate immune cell function, yet their specific roles in NK cells remain poorly characterized despite known effects on macrophages and lymphocytes.Objective: This review aims to consolidate current knowledge on the involvement of lncRNAs in NK cell biology, focusing on their regulatory impact on NK cell development, effector functions, and interactions within the tumor microenvironment (TME).Methods: We conducted a comprehensive narrative review of the literature, synthesizing findings related to lncRNA expression and function in hematopoiesis, NK cell maturation, cytotoxicity, cytokine production, and immune checkpoint modulation.Results: Our analysis reveals that lncRNAs are emerging as critical regulators across multiple stages of NK cell biology. They influence hematopoietic differentiation, modulate NK cell development and maturation, and directly affect cytotoxic degranulation and cytokine secretion. Importantly, lncRNAs are implicated in NK cell suppression within the TME, where they modulate immune checkpoint pathways and can either enhance or diminish the anti-tumor response.Conclusion: Elucidating the specific roles of lncRNAs in NK cells is crucial for a deeper understanding of the NK cell microenvironment. These insights hold significant potential for the development of novel NK cell-based immunotherapies and the identification of new biomarkers for cancer diagnosis and prognosis.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-22"},"PeriodicalIF":2.3,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470349","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

Bacteria Colonization is Associated with Inflammation-Antigen Presentation Imbalance in Myeloid Cells and Tumor Microenvironment Features in Melanoma. 黑素瘤中细菌定植与髓系细胞炎症-抗原呈递失衡和肿瘤微环境特征相关

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-15 DOI: 10.1080/08820139.2026.2702079

Ziqi Gong, Wenhui Guo, Ziyi Zhang, Haizhen Du, Xiaowen Wu, Jing Tu

{"title":"Bacteria Colonization is Associated with Inflammation-Antigen Presentation Imbalance in Myeloid Cells and Tumor Microenvironment Features in Melanoma.","authors":"Ziqi Gong, Wenhui Guo, Ziyi Zhang, Haizhen Du, Xiaowen Wu, Jing Tu","doi":"10.1080/08820139.2026.2702079","DOIUrl":"https://doi.org/10.1080/08820139.2026.2702079","url":null,"abstract":"Background: Intracellular microbes have been detected in multiple tumors, but their impact on the tumor microenvironment of melanoma and immune regulation remains unclear.Methods: We applied single-cell host-microbe interaction analysis to single cell RNA sequencing data from 42 melanoma samples to characterize host-microbe interactions. Multiple functional annotation approaches were integrated to assess immune and tumor cell transcriptional states associated with bacteria colonization.Results: Intracellular bacteria, particularly human-colonizing bacteria were associated with distinct transcriptional alterations in the tumor immune microenvironment, characterized by increased inflammation and reduced antigen presentation signatures in myeloid cells, along with enhanced innate immune-related transcriptional patterns, whereas adaptive T cell-related immune signatures were reduced. Tumor cells also exhibited transcriptional alterations, including increased metabolic activity and extracellular matrix remodeling pathways. At the bulk transcriptomic level, colonizing bacteria-associated chronic inflammatory features were correlated with increased CD8+ T cell infiltration and improved overall survival, while also showing a potential association with responses to immunotherapy.Conclusions: Intracellular colonizing bacteria were associated with inflammation-antigen presentation imbalance in melanoma tumor microenvironment.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-25"},"PeriodicalIF":2.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148455660","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 Dual Role of TLR2 in Breast Cancer: Implications for Therapeutic Targeting. TLR2在乳腺癌中的双重作用：治疗靶向的意义。

IF 2.3 4区医学

Immunological Investigations Pub Date : 2026-07-14 DOI: 10.1080/08820139.2026.2698759

Hao Yu, Yang Zhang, Tianying Du, Shubo Zuo

{"title":"The Dual Role of TLR2 in Breast Cancer: Implications for Therapeutic Targeting.","authors":"Hao Yu, Yang Zhang, Tianying Du, Shubo Zuo","doi":"10.1080/08820139.2026.2698759","DOIUrl":"https://doi.org/10.1080/08820139.2026.2698759","url":null,"abstract":"Background: Breast cancer (BC) remains a leading cause of cancer-related mortality because of its molecular heterogeneity, recurrence, and resistance to systemic therapies. Toll-like receptor 2 (TLR2) has emerged as a key regulator of both tumor cell signaling and the tumor microenvironment, making it a promising therapeutic target.Objective: This review summarizes the biological functions, clinical significance, and therapeutic potential of TLR2 in BC, with emphasis on its context-dependent effects across different cellular compartments.Methods: We reviewed current experimental and clinical evidence on TLR2 signaling, expression patterns, immune regulation, and therapeutic targeting in BC, integrating findings from tumor biology, immunology, and translational studies.Results: TLR2 signals primarily through the TIRAP/MYD88 pathway to activate NF-κB, MAPK, and, under specific conditions, IRF7-related pathways. Its biological effects depend on molecular subtype, ligand source, cellular context, and activation kinetics. Persistent TLR2 activation in tumor cells, cancer stem-like cells, suppressive myeloid cells, fibroblasts, and metastatic niches promotes stemness, epithelial-mesenchymal transition, metastasis, therapeutic resistance, and immune evasion. Conversely, selective activation in conventional type 1 dendritic cells and appropriately polarized macrophages enhances antigen presentation, cytotoxic T-cell priming, and antitumor immunity.Conclusions: TLR2 functions as a context-dependent immune-state switch rather than a uniformly pro-or antitumor receptor. Biomarker-guided strategies that selectively inhibit tumor-promoting TLR2 signaling while preserving or enhancing immune-activating functions may improve precision immunotherapy for BC.","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-31"},"PeriodicalIF":2.3,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148436552","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

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