Immunological Investigations最新文献

{"title":"Astragalus Polysaccharide Promotes NLRP3⁺ Macrophages Polarization via Suppression of OGT in Hepatocellular Carcinoma.","authors":"Yaping Lv, Mingyun Ma, Xiaobo Zhu, Lingling Xv, Boqi Song, Pan Cheng, Qiang Huang, Chun Li","doi":"10.1080/08820139.2026.2645964","DOIUrl":"10.1080/08820139.2026.2645964","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is characterized by an immunosuppressive tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs). Astragalus polysaccharide (APS) exhibits anti-tumor activity, its mechanism in reprogramming immunosuppressive TAMs remains unclear.</p><p><strong>Methods: </strong>We established a subcutaneous HCC tumor model in C57BL/6 mice and administered APS. Single-cell RNA sequencing (scRNA-seq) was performed to profile immune cell landscapes in HCC TME. Flow cytometry, immunofluorescence, and functional assays were employed to explore the role of O-linked N-acetylglucosamine transferase (OGT) in APS-mediated TME reprogramming.</p><p><strong>Results: </strong>APS significantly inhibited tumor growth and remodeled the TME cellular composition. ScRNA-seq revealed 10 cell types in HCC mice tumor tissue. APS increased neutrophils, macrophages, and mast cells while reducing other immune populations. Macrophages were subclassified into C1QC⁺ TAM, NLRP3⁺ TAM, and S100A9⁺ TAM. APS specifically elevated NLRP3⁺ TAM abundance, which positively correlated with M1-like pro-inflammatory phenotypes (TNFα, complement pathway activation). Mechanistically, APS downregulated OGT expression and global O-GlcNAcylation in TAMs, promoting NLRP3⁺ TAM polarization. NLRP3⁺ TAMs with APS treatment secreted pro-inflammatory cytokines and chemokines (IL-6, IL-1B, TNFα, and CXCL10), enhancing CD8⁺ T-cell infiltration and reducing T-cell exhaustion.</p><p><strong>Conclusion: </strong>APS suppresses HCC by inhibiting OGT-mediated O-GlcNAcylation and promoting NLRP3⁺ M1-like TAMs enrichment, thereby enhancing anti-tumor immunity, highlighting APS as a potential immunomodulatory agent for HCC therapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"750-773"},"PeriodicalIF":2.3,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147511677","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}

{"title":"CD36-Mediated Fatty Acid Oxidation in CTCs Drives Immune Evasion and Metastasis in NSCLC.","authors":"Huizhen Zhu, Shuiyan Dai, Fengping Wang, Shuai Qian","doi":"10.1080/08820139.2026.2619575","DOIUrl":"10.1080/08820139.2026.2619575","url":null,"abstract":"<p><strong>Background: </strong>Immune checkpoint inhibitors (ICIs) show clinical benefit in subsets of non-small cell lung cancer (NSCLC) patients, yet resistance remains a major challenge. Circulating tumor cells (CTCs) contribute to tumor dissemination and immune regulation. This study investigated the metabolic features of CTC subpopulations under PD-1 resistance, with a focus on the role of CD36⁺CTCs in immune evasion and pre-metastatic niche (PMN) formation.</p><p><strong>Methods: </strong>PD-1-resistant in vitro and murine NSCLC models were established to enrich and isolate CTCs. CD36⁺ CTCs were characterized using lipid metabolomics, RNA sequencing, and functional assays. Their roles in PMN formation and immune suppression were evaluated using lung metastasis models and a tri-cell co-culture system. Fatty acid oxidation (FAO) dependency was assessed by lipid imaging, mitochondrial activity analysis, and pharmacological inhibition with etomoxir.</p><p><strong>Results: </strong>CD36⁺ CTCs were enriched under PD-1 resistance and exhibited enhanced lipid accumulation, increased mitochondrial activity, and FAO dependency. Multi-omics analyses revealed activation of lipid metabolic pathways associated with immune suppression and extracellular matrix remodeling. Functionally, CD36⁺ CTCs promoted PMN formation and inhibited T-cell activation, while FAO inhibition significantly reduced their migratory and metastatic potential.</p><p><strong>Conclusion: </strong>CD36⁺ CTCs drive immune evasion and metastasis in PD-1-resistant NSCLC through FAO-dependent metabolic reprogramming. Targeting this metabolic vulnerability may enhance the efficacy of immunotherapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"563-601"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201455","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}

{"title":"\"Targeting the Body Itself\": Research Progress on the Anti-Inflammatory and Immunomodulatory Mechanisms of Traditional Chinese Medicine Based on Pyroptosis Theory.","authors":"Xiaobing Ma, Peihui Han, Kanghong He, Guangnan Wang, Yiling Lu","doi":"10.1080/08820139.2026.2618636","DOIUrl":"10.1080/08820139.2026.2618636","url":null,"abstract":"<p><strong>Background: </strong>Pyroptosis is a highly inflammatory form of regulated cell death executed by gasdermin proteins. It promotes the release of interleukin (IL)-1β and IL-18 to support host defense, yet its dysregulation contributes to sepsis, neurodegenerative disorders, and autoimmune diseases. Many current anti-inflammatory therapies are single-target and may not restore system-level immune balance.</p><p><strong>Objective: </strong>To summarize core pyroptosis pathways and evaluate how Traditional Chinese Medicine (TCM) modulates pyroptosis through multi-component, multi-target regulation.</p><p><strong>Methods: </strong>We synthesize mechanistic evidence on canonical and non-canonical inflammasome cascades, focusing on caspase activation and Gasdermin D (GSDMD) cleavage. We further summarize data on representative TCM-derived compounds (berberine, curcumin, ginsenoside Rd) and a classical formula (Buyang Huanwu Decoction), emphasizing their actions on key pyroptosis nodes and upstream stress signals.</p><p><strong>Results: </strong>Pyroptosis is driven by inflammasome-dependent signaling that activates caspases, cleaves GSDMD, and triggers pore formation with inflammatory mediator release. Evidence suggests TCM interventions can attenuate pyroptosis by converging on NLRP3 inflammasome activation, NF-κB/STAT3 signaling, and mitochondrial reactive oxygen species, while formulas may provide broader antioxidant and intercellular regulatory effects.</p><p><strong>Conclusion: </strong>TCM offers a systems-oriented strategy for pyroptosis-centered anti-inflammatory and immunomodulatory therapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"666-695"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146179446","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}

{"title":"Naloxone and Naltrexone as Potential Adjuvants for Vaccination Against Intracellular Pathogens: A Narrative Review.","authors":"Hajar Yaghoobi, Maryam Hataminejad, Hakim Azizi","doi":"10.1080/08820139.2025.2607684","DOIUrl":"10.1080/08820139.2025.2607684","url":null,"abstract":"<p><strong>Background: </strong>Adjuvants potentiate adaptive immunity by enhancing antigen-specific immune responses, yet many exhibit high toxicity for clinical use. Naloxone (NLx) and naltrexone (NLt) opioid receptor antagonists have emerged as promising adjuvants in preclinical vaccination models against intracellular pathogens.</p><p><strong>Objective: </strong>This narrative review synthesizes evidence from 2000 to 2025 evaluating NLx/NLt as adjuvants against bacterial, viral, and parasitic infections, while examining proposed immunoregulatory mechanisms.</p><p><strong>Methods: </strong>A comprehensive search of Web of Science, PubMed, Scopus, ScienceDirect, and ProQuest employed Boolean operators combining: (vaccine OR vaccination) AND (adjuvant) AND (naloxone OR naltrexone OR NLx OR NLt OR \"opioid receptor antagonist\") AND (\"immune response\" OR \"cellular immunity\" OR \"Th1\").</p><p><strong>Results: </strong>Key findings demonstrate that NLx/NLt monotherapy or combinatorial use with Alum consistently, enhanced Th1 polarization and cellular immunity, Elevated pathogen clearance and protection rates, synergistically overcame Alum's Th2 bias. Mechanistically, μ-opioid receptor (MOR) antagonism disrupts tonic immunosuppression, reversing opioid-mediated inhibition of dendritic cell maturation, IL-12 production, and cytotoxic T-cell function.</p><p><strong>Conclusions: </strong>This immunorestorative action positions NLx/NLt as strategic adjuvants for vaccines targeting intracellular pathogens requiring robust cell-mediated immunity. Future horizons include combinatorial platforms (e.g. DNA vaccines + low-dose naltrexone) and clinical translation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"638-665"},"PeriodicalIF":2.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888594","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}

{"title":"Exosomal miR-451a Derived from Bone Marrow Mesenchymal Stem Cells Inhibits Macrophage M1 Polarization Through the MIF/CD74 Signaling Pathway to Alleviate Acute Lung Injury.","authors":"Lisi Luo, Wensha Nie, Ji Wang, Yongze Liu, Qinglang Dai, Yuan Liao, Feng Li","doi":"10.1080/08820139.2026.2615654","DOIUrl":"10.1080/08820139.2026.2615654","url":null,"abstract":"<p><strong>Background: </strong>Macrophage polarization is widely involved in the progression of acute lung injury (ALI). Bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exos) have been reported to participate ininflammatory diseases by regulating macrophage polarization. This study aimed to investigate the role of BMSC-Exos in ALI through the regulation of macrophage polarization.</p><p><strong>Methods: </strong>LPS-induced ALI mouse models and RAW264.7 cell injury models were established. Lung injury was assessed through HE staining and assessment of bronchoalveolar lavage fluid (BALF) protein contents, the lung wet/dry weight ratios, and lung myeloperoxidase (MPO) activities. The expression of protein was detected via Western blotting and immunofluorescence. Exosomes were characterized using transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA).</p><p><strong>Results: </strong>BMSC-Exos significantly alleviated pathological lung injury in ALI mice; reduced the lung wet/dry weight ratio, BALF protein content, MPO activity. BMSC-Exos inhibited LPS-induced macrophage M1 polarization and reduced proinflammatory cytokine expression. The molecular mechanism revealed that the BMSC-Exos delivered miR-451a to the macrophages and that inhibition of miR-451a expression attenuated the suppressive effect of the BMSC-Exos on M1 polarization. Furthermore, miR-451a targeted MIF to inhibit the MIF/CD74 signaling pathway.</p><p><strong>Conclusion: </strong>BMSC-Exos inhibit MIF/CD74 signaling by delivering miR-451a, thereby suppressing LPS-induced M1 macrophage polarization and alleviating ALI.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"519-540"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145998058","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}

{"title":"Emerging Immunotherapeutic Approaches in Colorectal Cancer: From Checkpoint Inhibitors to CAR-T Cell and Viral Vector Vaccines.","authors":"Rajeev Ranjan, Amit Kumar, Vikas Kumar, Bhawesh Kumar Mahato, Atreyee Sarkar, Ratnesh Kumar Yadav, Vikas Gond, Sreeharsha Nagaraja, Ravi Raj Pal","doi":"10.1080/08820139.2026.2613047","DOIUrl":"10.1080/08820139.2026.2613047","url":null,"abstract":"<p><strong>Introduction: </strong>Colorectal Cancer has been a significant health issue at a global level in terms of increasing incidence, high metastatic capacity, and inadequate treatment reactions in most patient groups. Though chemotherapy and targeted agents have given better survival chances, resistance to treatment, avoidance of the immune system as well as systemic toxicity still limit long-term efficacy. Immunotherapeutic strategies have developed as effective methods in the past few years to address these shortomings.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted across different electronics databases including Web of Science, PubMed, Scopus, and ScienceDirect utilizing keywords colorectal cancer immunotherapy, PD-1 / PD-L1, CAR-T cells, viral vector vaccines, carcinoembryonic antigen alone and in combinations.</p><p><strong>Results: </strong>PD-1/PD-L1, CTLA-4, immune checkpoint inhibitors have shown long-term responses, especially in mismatch repair-deficient and microsatellite instability-high tumours, and cell-based therapies such as CAR -T cells and dendritic cell vaccines provide other opportunities of personalised immune modulation.</p><p><strong>Discussion: </strong>This critical review summarizes the current developments in terms of immunotherapy and interventions of CRC with a focus on the mechanistic understanding of the issue, clinical outcomes, and combinatorial strategies aimed to improve antitumor immunity and surmount therapy resistance. Specific attention is paid to the optimization of the checkpoint blockade, innovations with vaccines and CAR-T engineering to accumulate and release tumor-specific cells and control the microenvironment. Finally, key translational challenges current clinical trials, and future perspectives are identified to promote the development of the next-generation multimodal therapies in the efficient and customized management of CRC.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"602-637"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951844","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}

{"title":"PTBP1-TRAF6 Axis Aggravates Chronic Obstructive Pulmonary Disease by Promoting M1 Macrophage Polarization and Impairing Clearance of Neutrophil Extracellular Traps.","authors":"Mingming Zhao, Liangfeng Yang, Shanshan Xu, Gang Chen, Yanping Hang, Minmin Yang, Haixia Zheng, Miaomiao Kong, Tao Li, Nan Wang","doi":"10.1080/08820139.2025.2611872","DOIUrl":"10.1080/08820139.2025.2611872","url":null,"abstract":"<p><strong>Objective: </strong>To elucidate the role of the polypyrimidine tract-binding protein 1 (PTBP1)-tumor necrosis factor receptor-associated factor 6 (TRAF6) pathway in chronic obstructive pulmonary disease (COPD), with a particular focus on its regulatory effects on macrophage polarization and clearance of neutrophil extracellular traps (NETs).</p><p><strong>Methods: </strong>A COPD-like mouse model was established via cigarette smoke (CS) exposure. Lung injury, macrophage polarization, and levels of NETs were assessed. The role of TRAF6 in macrophage polarization and NETs clearance was assessed through lentiviral modulation of TRAF6 expression. RNA immunoprecipitation-quantitative polymerase chain reaction (RIP-qPCR), RNA stability assays, and Western blotting were performed to investigate the regulatory mechanism of PTBP1 on TRAF6 expression.</p><p><strong>Results: </strong>The COPD-like mouse model exhibited increased M1 and decreased M2 macrophage populations, along with elevated NETs formation. Both PTBP1 and TRAF6 were upregulated in lung tissues of the COPD-like mouse model and cigarette smoke extract (CSE)-treated macrophages. Mechanistically, PTBP1 bound to and stabilized TRAF6 mRNA, enhancing TRAF6 expression. Inhibition of the PTBP1-TRAF6 pathway alleviated lung injury, restored macrophage polarization balance, and promoted NETs clearance.</p><p><strong>Conclusion: </strong>PTBP1 enhances TRAF6 expression by stabilizing its mRNA, promoting M1 macrophage polarization and impairing NETs clearance, ultimately aggravating COPD.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"493-518"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951816","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}

{"title":"Correction.","authors":"","doi":"10.1080/08820139.2026.2619328","DOIUrl":"10.1080/08820139.2026.2619328","url":null,"abstract":"","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"696"},"PeriodicalIF":2.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018408","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}

{"title":"Propofol Inhibits HIF-1α/NLRP3 Signaling Pathway and Mast Cell Activation to Ameliorate Airway Inflammation in Allergic Asthma.","authors":"Yuzhu Zhang, Jiangling Xia, Xiaona An, Luning Chen, Zhenzhen Chen","doi":"10.1080/08820139.2026.2618136","DOIUrl":"10.1080/08820139.2026.2618136","url":null,"abstract":"<p><strong>Background: </strong>The objective was to assess the effects of propofol on ovalbumin (OVA)-induced asthma in a mouse model and the efficacy of propofol in stabilizing mast cells and inhibiting the production of inflammatory mediators.</p><p><strong>Methods: </strong>Animal model of asthma induced by OVA was employed to evaluate the effect of propofol. Tissues from the lungs were retrieved for HE staining. The levels of IgE, IFN-γ, MPO, and so on was deteced. Bone marrow mast cells (BMMCs) were isolated to examine the suppressive action of propofol on the degranulation.</p><p><strong>Results: </strong>Propofol significantly reduced airway hyperresponsiveness and IgE, Th2 cytokines, and inflammatory cytokines in OVA-induced asthma model. Inhibited BMMCs degranulation and the production of inflammatory cytokines. Additionally, propofol inhibited the expression of HIF-1α and NLRP3 in asthma models. Overexpression HIF-1α in BMMCs reverses the effect of propofol. NLRP3 inhibition attenuates allergic asthma in DNP-HSA-treated DMMCs with or without overexpression HIF-1α. In terms of the mechanism, propofol interacts with HIF-1α directly, thereby disrupting HIF-1α-NLRP3 interaction and attenuating allergic asthma.</p><p><strong>Conclusion: </strong>Propofol markedly improved OVA-induced asthma and inhibited mast cell degranulation by binding competitively to HIF-1α, thereby disrupting the HIF-1α-NLRP3 interaction and attenuating allergic asthma.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":"55 3","pages":"541-562"},"PeriodicalIF":2.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467929","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}

{"title":"The Role of Myeloid-Derived Suppressor Cell (MDSC) in Fungal Infections and Its Potential as a Therapeutic Target.","authors":"Mahdi Ghasempour, Parisa Zafari","doi":"10.1080/08820139.2025.2583275","DOIUrl":"10.1080/08820139.2025.2583275","url":null,"abstract":"<p><strong>Background: </strong>The interaction between the immune system and fungi has long intrigued researchers, as fungi are among the most common organisms encountered by humans. Myeloid-derived suppressor cells (MDSCs) are specialized immune cells that play a key role in modulating immune responses during fungal infections by inhibiting T-cell activity.</p><p><strong>Objectives: </strong>This review aims to investigate the mechanisms by which MDSCs influence fungal infections and to explore their potential as therapeutic targets.</p><p><strong>Methods: </strong>A comprehensive review of existing studies examining MDSC activity in various fungal infections was conducted. Comparative analysis focused on the protective versus non-protective effects of MDSCs across different fungal species.</p><p><strong>Results: </strong>MDSCs suppress pro-inflammatory T-cell responses, leading to two contrasting outcomes. On one hand, this suppression mitigates disease progression by reducing harmful inflammation. On the other, it can enhance fungal survival by preventing T-cell-mediated damage. Protective effects of MDSCs have been observed in <i>Candida albicans</i> infections, whereas non-protective or detrimental effects have been reported in infections caused by <i>Candida tropicalis</i>, <i>Paracoccidioides</i>, <i>Aspergillus fumigatus</i>, <i>Cryptococcus neoformans</i>, <i>Malassezia</i>, and <i>Mucor</i> species.</p><p><strong>Conclusions: </strong>MDSCs play a dual role in fungal infections, balancing protective immune regulation with facilitation of fungal persistence. Understanding their mechanisms offers promising avenues for the development of targeted immunotherapies against fungal pathogens.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"333-351"},"PeriodicalIF":2.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145437818","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}