Immunological Investigations最新文献

{"title":"Decoding Functional Plasticity of γδ T Cells in Mosquito-Borne Diseases.","authors":"Feileyang Xie, Qingyuan Cheng, Liman Li","doi":"10.1080/08820139.2026.2724898","DOIUrl":"https://doi.org/10.1080/08820139.2026.2724898","url":null,"abstract":"<p><strong>Background: </strong>Mosquito‑borne diseases (MBDs), caused by pathogens including dengue virus (DENV), West Nile virus (WNV), Zika virus (ZIKV), chikungunya virus (CHIKV) and \"Plasmodium\" species, pose a major global health threat with limited effective interventions. As a distinctive T‑cell subset, γδ T cells exert crucial immunoregulatory functions during infection owing to their unique tissue distribution and functional plasticity, yet their roles in MBDs remain incompletely understood.</p><p><strong>Objectives: </strong>This review summarizes the immunoregulatory mechanisms of γδ T cells in MBDs and discusses their potential as immunotherapeutic targets.</p><p><strong>Methods: </strong>A systematic literature search was performed in PubMed using keywords such as \"γδ T cells\", \"Plasmodium\", \"dengue virus\" and \"Zika virus\". Relevant publications up to March 2026 were comprehensively reviewed.</p><p><strong>Results: </strong>γδ T cells display dual protective and pathogenic effects across MBDs. They mainly confer protection against Plasmodium and CHIKV infections, while drive pathological responses in DENV and ZIKV infections. In WNV infection, γδ T cells activate immune cells and simultaneously induce blood‑brain barrier damage.</p><p><strong>Conclusions: </strong>γδ T cells exert multifaceted functions in MBDs. Elucidating their functional plasticity may provide insights for developing targeted immunotherapies against MBDs.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962950","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":"Single-Cell Transcriptomics Uncovers β-Elemene-Induced Macrophage Reprogramming as a Mechanism to Suppress Osteosarcoma Stemness via the CCL2-Akt Axis.","authors":"Shaochun Zhang, Ting Liu, Jing Ke","doi":"10.1080/08820139.2026.2696497","DOIUrl":"https://doi.org/10.1080/08820139.2026.2696497","url":null,"abstract":"<p><strong>Background: </strong>β-elemene (ELE), a natural sesquiterpene with antitumor properties, exerts immunomodulatory effects on osteosarcoma (OS), but its impact on the tumor microenvironment and cancer stemness remains unclear. This study investigated how ELE reprograms tumor-associated macrophages (TAMs) to suppress OS progression.</p><p><strong>Methods: </strong>We combined single-cell RNA sequencing (scRNA-seq) of a murine OS model with functional validations, including macrophage polarization assays, co-culture systems, western blot, RT-PCR, ELISA, tumorsphere formation, and rescue experiments (CCL2 overexpression, Akt activation).</p><p><strong>Results: </strong>ELE treatment significantly inhibited OS tumor growth and promoted apoptosis. scRNA-seq revealed that ELE skewed TAMs from immunosuppressive M2 to antitumor M1 phenotypes, concurrently reducing the osteosarcoma stem-like cell (OSC) population. Cell communication analysis showed enhanced M1-OSC pro-inflammatory signaling (e.g. TNF, IL-1) and suppressed M2-derived CCL2 signaling. Mechanistically, ELE downregulated CCL2 secretion from M2 macrophages, inhibiting Akt phosphorylation and subsequent β-catenin activation, which led to reduced expression of stemness markers (SOX2, NANOG, CD133) and impaired OSC self-renewal and invasion. These effects were reversed by CCL2 overexpression or Akt activation.</p><p><strong>Conclusion: </strong>ELE attenuates OS stemness by polarizing TAMs toward an M1 phenotype and disrupting the CCL2/Akt/β-catenin axis, revealing a novel immunometabolic mechanism for OS therapy.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-30"},"PeriodicalIF":2.3,"publicationDate":"2026-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148955846","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":"Immunometabolic Reprogramming as a Therapeutic Platform: Integrating Systems Immunology with Precision Biopharmaceutical Engineering.","authors":"Hosein Yousefi, Cobra Moradian","doi":"10.1080/08820139.2026.2731116","DOIUrl":"https://doi.org/10.1080/08820139.2026.2731116","url":null,"abstract":"<p><strong>Introduction: </strong>Immunometabolism integrates energy demands, biosynthesis, redox homeostasis, and immune-cell function, yet metabolic phenotypes remain context dependent. This review conceptualizes immunometabolic reprogramming as a multiscale regulatory network connecting microenvironmental pressures, nutrient sensing, metabolic flux, metabolite-mediated regulation, immune-cell states, systems-level biomarkers, and precision therapeutic engineering.</p><p><strong>Methods: </strong>A structured narrative review synthesized literature published from January 2022 onward across five domains: microenvironmental metabolic control; metabolic signaling and pathway interactions; systems immunology and biomarker discovery; engineered therapeutic platforms; and translational evidence, safety, and patient stratification. Quantitative findings were retained only when their experimental context supported interpretation.</p><p><strong>Results: </strong>Oxygen, nutrient, pH, cytokine, and metabolite availability can reshape AMPK, mTOR, HIF-1α, and related signaling, thereby altering glycolytic, mitochondrial, lipid, amino-acid, and redox metabolism. These changes interact with transcriptional and epigenetic mechanisms to regulate immune-cell states. Systems-level profiling enables biomarker development, while engineered biologics, targeted delivery systems, extracellular-vesicle platforms, and metabolically conditioned immune cells offer emerging therapeutic opportunities. However, translational maturity varies substantially across interventions.</p><p><strong>Conclusion: </strong>Immunometabolic reprogramming should be interpreted as a context-dependent network rather than a collection of isolated pathways. Clinical translation requires evidence-graded interventions, tissue- and dose-aware strategies, validated biomarkers, and patient stratification to distinguish established benefit from promising but unproven engineering approaches.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929809","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":"NK and CIK Cells in Hematologic Malignancies: Comparative Mechanisms, Clinical Evidence, and Translational Perspectives.","authors":"Shiva Mosadegh Manshadi, Ghazaleh Sankanian, Mohammadreza Moshari, Abbas Hajifathali, Elham Roshandel, Saeid Kaviani Jabali","doi":"10.1080/08820139.2026.2713766","DOIUrl":"https://doi.org/10.1080/08820139.2026.2713766","url":null,"abstract":"<p><strong>Background: </strong>Hematologic malignancies remain a major cause of morbidity and mortality despite advances in chemotherapy, targeted therapies, and hematopoietic stem cell transplantation. Adaptative cell therapy has emerged as a promising approach, in which natural killer (NK) and cytokine-induced killer (CIK) cells appear as potentially complementary effective platforms.</p><p><strong>Objective: </strong>This review critically compares NK and CIK cells as two adaptive cellular immunotherapy platforms for hematologic malignancies, focusing on their biological properties, antitumor mechanisms, production strategies, clinical evidence, safety profiles, and translational limitations.</p><p><strong>Methods: </strong>NK and CIK cells were comparatively evaluated with respect to their biological properties, antitumor mechanisms, production strategies, clinical evidence, safety profiles, and translational limitations.</p><p><strong>Results: </strong>NK cells, through the release of perforin-granzyme, death receptor pathways, and antibody-dependent cytotoxicity, perform rapid tumor clearance, allowing for immediate tumor volume reduction, but with limited persistence in vivo. In contrast, in vitro-expanded CIK cells (CD3+CD56+) show robust proliferation and sustained cytotoxicity, with an overall low, but not entirely zero, risk of graft-versus-host disease, supporting long-term immune surveillance. CAR engineering, cytokine-induced memory-like NK cells, and DC-CIK platforms may improve persistence, specificity, and metabolic fitness. Combination strategies with checkpoint inhibitors and standard therapies may enhance antitumor efficacy. However, most evidence is still preliminary and comes mainly from early-phase, single-arm, and heterogeneous studies.</p><p><strong>Conclusions: </strong>NK and CIK cells may offer complementary benefits rather than direct competitive approaches. Their distinct functional properties provide the biological rationale for future combination or sequential strategies. However, prospective clinical studies are needed to define their efficacy, safety, durability, and optimal clinical application in hematological malignancies.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-35"},"PeriodicalIF":2.3,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929824","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":"IgG4 and Rheumatoid Arthritis: A Comprehensive Review of Its Role in Inflammation, Biomarker Potential, and Therapeutic Implications.","authors":"Li Zhang, Haili Shen, Yuan Li","doi":"10.1080/08820139.2026.2729080","DOIUrl":"https://doi.org/10.1080/08820139.2026.2729080","url":null,"abstract":"<p><strong>Background: </strong>Immunoglobulin G4 (IgG4) is the least abundant IgG subclass and has distinctive structural and functional properties, including Fab-arm exchange and limited activation of antibody-dependent effector mechanisms. These features contribute to its generally non-inflammatory and tolerogenic profile. However, the role of IgG4 in rheumatoid arthritis (RA) remains incompletely understood.</p><p><strong>Objective: </strong>This review aims to summarize and critically evaluate the biological characteristics of IgG4, its clinical significance in RA, and the potential therapeutic implications of IgG4-mediated immune responses.</p><p><strong>Evidence: </strong>Elevated serum IgG4 levels have been reported in a subset of patients with RA and have been associated with disease activity, inflammatory markers, autoantibody levels, and treatment response in some studies. IgG4 autoantibodies, including antinuclear IgG4 antibodies, have also been detected in autoimmune diseases and may influence complement activation and proinflammatory cytokine production. However, findings remain heterogeneous, and current evidence is insufficient to establish IgG4 as an independent diagnostic or prognostic biomarker in routine RA care.</p><p><strong>Conclusion: </strong>IgG4 may have a complex, context-dependent role in RA, potentially reflecting both immune dysregulation and compensatory anti-inflammatory responses. Further research is needed to clarify its pathogenic mechanisms, clinical utility, and potential as a therapeutic target.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919674","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":"Toll-Like Receptor 3 Inhibition Reduces Vasoconstriction and Blood Pressure in Spontaneously Hypertensive Rats via COX-1 Downregulation.","authors":"Taynara Santos Santana, Vanessa Dela Justina, Raiany Alves de Freitas, Kenia Pedrosa Nunes, Fernanda Regina Giachini Vitorino, Victor Vitorino Lima","doi":"10.1080/08820139.2026.2731120","DOIUrl":"https://doi.org/10.1080/08820139.2026.2731120","url":null,"abstract":"<p><strong>Background: </strong>Toll-like receptors (TLRs) are implicated in blood pressure (BP) regulation, but the role of TLR3 in hypertension remains poorly understood. We hypothesized that anti-TLR3 treatment reduces vasoconstriction and lowers BP in hypertension.</p><p><strong>Methods: </strong>To test this, spontaneously hypertensive rats (SHR) and normotensive Wistar controls were treated with either IgG or an anti-TLR3 antibody. BP was measured, and mesenteric arteries were assessed for vascular reactivity, protein expression, and histology.</p><p><strong>Results: </strong>Anti-TLR3 treatment significantly reduced BP in SHR. It also decreased the contractile response to noradrenaline, an effect abolished by indomethacin, and prevented the increased COX-1 expression in SHR while reducing COX-2 expression in both strains. Furthermore, anti-TLR3 reduced collagen I and increased collagen III deposition in the mesenteric artery and lowered TLR3 expression in the tunica media of SHR.</p><p><strong>Conclusion: </strong>These findings support TLR3 may represent a novel therapeutic target in hypertension.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148919688","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":"Epigenetic Regulation of Host Immunity During Parasitic Infections: Mechanisms, Immune Evasion, and Therapeutic Opportunities.","authors":"Hind Alzaylaee, Walaa A Elkholy, Marwa A Elkholy, Rewaida Abdel-Gaber, Duaa Eliwa, Hoda A A Shaheen, Gaber El-Saber Batiha","doi":"10.1080/08820139.2026.2729085","DOIUrl":"https://doi.org/10.1080/08820139.2026.2729085","url":null,"abstract":"<p><strong>Introduction: </strong>Parasitic infections remain a major global health challenge involving complex interactions between pathogens and host immunity. Emerging evidence indicates that epigenetic mechanisms, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, critically regulate immune responses and influence host susceptibility, resistance, and disease progression.</p><p><strong>Methods: </strong>This review synthesizes current evidence on epigenetic regulation of host immunity during parasitic infections, focusing on mechanisms underlying immune activation, immune evasion, host susceptibility, and parasite persistence. Emerging epigenetic biomarkers and therapeutic strategies targeting epigenetic pathways are also considered.</p><p><strong>Results: </strong>Parasites can manipulate host epigenetic machinery to evade immune surveillance, suppress protective responses, and establish persistent infections. Conversely, epigenetic regulation in immune cells modulates cytokine production, macrophage polarization, T-cell differentiation, and immune memory, thereby influencing infection outcomes. Parasite-derived epigenetic factors and non-coding RNAs may additionally contribute to immune modulation and immunopathology. Epigenetic signatures associated with disease severity and treatment response show potential as biomarkers, while targeting epigenetic pathways may enhance antiparasitic immunity.</p><p><strong>Discussion: </strong>Epigenetic regulation represents a central mechanism governing host-parasite interactions. Integrating advanced approaches, including single-cell epigenomics and spatial transcriptomics, may clarify cell-specific mechanisms and identify novel biomarkers and therapeutic targets. These advances could support personalized strategies to improve antiparasitic treatment and disease outcomes.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-45"},"PeriodicalIF":2.3,"publicationDate":"2026-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148906010","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":"Complement Factor H Regulates a Complement-Extracellular Vesicle-Macrophage Axis in Immune Mediated Kidney Injury.","authors":"Aum Campanieri, Shane Fraher, Poolakkad S Satheeshkumar, Jessica Reynolds, Richard J Quigg, Jessy J Alexander","doi":"10.1080/08820139.2026.2718198","DOIUrl":"https://doi.org/10.1080/08820139.2026.2718198","url":null,"abstract":"<p><p><b>Introduction:</b> Complement Factor H (FH) regulates the alternative complement pathway, and FH deficiency promotes complement activation, macrophage recruitment, and renal injury. Extracellular vesicles (EVs) mediate intercellular communication and may provide molecular signatures of tissue inflammation.<b>Methods:</b> We examined complement- and macrophage-associated transcriptional signatures in renal tissue and serum-, kidney-, and urine-derived EVs using a FH-deficient murine model of chronic serum sickness. Pilot kidney microarray analysis was combined with qRT-PCR and EV transcript profiling.<b>Results:</b> FH deficiency increased renal expression of macrophage-associated inflammatory genes, including AIF1, MMP9, S100A10, and CD44, and the complement receptor C3aR1. EVs from FH-deficient mice lacked FH transcripts and exhibited increased complement- and macrophage-associated transcripts across serum-, kidney-, and urine-derived EV populations. EV transcriptional profiles paralleled inflammatory gene expression observed in renal tissue.<b>Discussion:</b> FH deficiency-associated complement dysregulation produces coordinated inflammatory transcriptional signatures detectable in both kidney tissue and EVs. The concordance between intrarenal inflammatory programs and EV cargo suggests that EVs may reflect complement-mediated renal immune activity. In particular, urinary EVs may provide a non-invasive source of molecular information and potential biomarkers of complement-mediated kidney inflammation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-16"},"PeriodicalIF":2.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900410","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 Expression of Notch1 and Notch2 is Up-Regulated on Natural Killer Cells by the Interaction Between NKp46 and Syndecan-1 in a Mouse Breast Cancer Model.","authors":"Lingying Wang, Tianmin Bie, Jiongming He, Yujie Xiao, Kang Chen","doi":"10.1080/08820139.2026.2729083","DOIUrl":"https://doi.org/10.1080/08820139.2026.2729083","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is characterized by uncontrolled breast cell growth and eventual tumor formation. It is crucial to explore the molecular mechanisms of NK cell function in the breast cancer microenvironment.</p><p><strong>Methods: </strong>The regulatory factors of Notch1 and Notch2 in NK cells were analyzed in a mouse breast cancer implantation model using flow cytometry, cytotoxicity evaluation, real-time PCR, in vitro co-culture, genetically modified tumor cells, and adoptive transfer of NK cells.</p><p><strong>Results: </strong>Notch1 and Notch2 were differentially expressed on tumor-infiltrating NK cells, forming a Notch1+Notch2+ (DP) subset and Notch1-Notch2-(DN) subset. DP cells expressed higher levels of IFN-γ, TNF-α, granzyme B, perforin, and CD107a upon activation, thereby becoming more cytotoxic. DP cells expressed higher levels of activating receptors, such as NKp46, NKG2D, and DNAM-1. Co-culture with the breast cancer cell line EMT6 up-regulated Notch1 and Notch2. Blockage of the ligation of NKp46 to its ligands prevented the up-regulation of Notch1 and Notch2. Moreover, NK cells expressed lower IFN-γ, TNF-α, Notch1, and Notch2 in Syndecan-1 (an NKp46 co-ligand) knockout EMT6 implants than their counterparts in Syndecan-1-expressing EMT6 implants, and were less competent to inhibit EMT6 implant growth.</p><p><strong>Conclusion: </strong>The NKp46-Syndecan-1 interaction promoted Notch1 and Notch2 expression to boost NK cell activity.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-19"},"PeriodicalIF":2.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900412","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":"Maternal Tuberculosis and Infant Gut and Immune Development: Implications for Maternal-Child Health.","authors":"Chioma Ohaeri, Débora Brito Gourlart, Ashiru Aliyu Zainulabidin, Aye Nyein Phyu, Mayowa Daniel Pemi, Abubakar Usman, Htin Lin Aung, Olabisi Flora Davies-Bolorunduro","doi":"10.1080/08820139.2026.2719706","DOIUrl":"https://doi.org/10.1080/08820139.2026.2719706","url":null,"abstract":"<p><strong>Background: </strong>Maternal tuberculosis (TB) during pregnancy involves chronic infection, immune activation, and antimicrobial therapy, which may alter the maternal gut, vaginal, and breast milk microbiomes and influence neonatal immune development.</p><p><strong>Methods: </strong>We conducted a narrative review of studies identified through PubMed and GoogleScholar addressing the maternal TB-microbiome-infant immunity axis. Where evidence from pregnant women with TB was limited, findings were extrapolated from non-pregnant TB populations, antibiotic exposure studies, and broader maternal-infant microbiome research.</p><p><strong>Results: </strong>Maternal TB and its treatment may alter gut, vaginal, and breast milk microbiomes and the immune-metabolic composition of milk. These changes could influence perinatal microbial transmission, mucosal maturation, and infant immune responses, including vaccine responsiveness, BCG immunogenicity, and IGRA conversion. Treatment timing, antibiotic exposure, and maternal nutrition may modify these effects.</p><p><strong>Conclusion: </strong>Understanding the maternal TB-microbiome-immune axis may help optimize infant immune outcomes. Longitudinal mother-infant studies, multi-omic analyses, and mechanistic models are needed to clarify these interactions and evaluate microbiome informed strategies, including nutritional optimization, targeted probiotics/prebiotics, and antibiotic stewardship.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-27"},"PeriodicalIF":2.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900419","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}