Immunological Investigations最新文献

{"title":"Immunomodulation by MSCs in Kidney Diseases: Molecular Mechanisms.","authors":"Yachao Li, Xinyi Fang, Xiang Gao, Chi Liu","doi":"10.1080/08820139.2026.2678469","DOIUrl":"https://doi.org/10.1080/08820139.2026.2678469","url":null,"abstract":"<p><p><b>Background:</b> Kidney disease progression is driven by immune dysregulation, inflammation, and fibrosis. Mesenchymal stem cells (MSCs) act via paracrine signaling (exosomes, IDO, PGE2, TGF-β) to modulate immunity.<b>Methods:</b> PubMed and Web of Science (2000-2026) were searched using keywords related to MSCs, kidney diseases, and the signaling pathways. Results: This review dissects molecular mechanisms by which MSCs regulate innate and adaptive immunity in kidney diseases. Focus is placed on specific intracellular cascades (NF-κB, NLRP3, PI3K-Akt, STAT, TGF-β/Smad, Wnt/β-catenin, cAMP-PKA, AhR, Nrf2, SIRT1·PGC-1α) and cell‑type responses (macrophages, tubular epithelial cells, podocytes, endothelial cells). Unlike broader reviews, we systematically explore cross-talk and compensatory interactions among pathways, and their shifting dominance from acute inflammation to chronic fibrosis.<b>Conclusions:</b> Critical gaps are identified: validation using conditional knockout models, exosome uptake routes, and rational MSC engineering. By integrating molecular‑resolution mechanisms, this review provides a foundation for pathway‑targeted, biomarker-guided MSC‑based therapies for kidney diseases.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-20"},"PeriodicalIF":2.3,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148900424","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":"Beyond the Bug: Reshaping the Immune Landscape - A New Era of Host-Directed Therapies for Tuberculosis.","authors":"Jing Zhao, Chao Wang, Nan Li, Jingmei Zhang","doi":"10.1080/08820139.2026.2719695","DOIUrl":"https://doi.org/10.1080/08820139.2026.2719695","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Tuberculosis (TB) remains a leading cause of infectious mortality worldwide. Although host inflammatory responses are essential for controlling Mycobacterium tuberculosis (Mtb), excessive or spatially dysregulated inflammation promotes granuloma necrosis, cavitation, tissue destruction, and transmission. Conventional antimicrobial therapy primarily targets the bacillus and does not directly resolve this host-pathogen paradox. Host-directed therapies (HDTs) are therefore evolving from broad immunomodulatory approaches, conceptualized here as HDT 1.0, toward mechanistically and spatially precise interventions, termed HDT 2.0.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;This narrative review examines the granuloma as an integrated pharmacologic target and proposes a next-generation framework for HDT development that addresses the spatial, metabolic, immunologic, and structural features that permit Mtb persistence and limit sterilizing therapy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Key findings: &lt;/strong&gt;Spatial transcriptomics, high-plex imaging, and advanced lesion profiling have revealed pronounced intralesional heterogeneity within TB granulomas, including avascular necrotic caseum, lipid-rich foamy macrophage zones, immune-excluded regions, and fibrotic cuffs. These microenvironments can restrict antibiotic penetration, impair T-cell trafficking and function, and create metabolically permissive niches for persistent bacilli. Accordingly, HDT 2.0 should address three interconnected therapeutic bottlenecks: improving drug access to poorly vascularized caseous lesions, disrupting lipid-dependent metabolic sanctuaries, and restoring spatially effective adaptive immunity without exacerbating immunopathology. Emerging approaches include spatially restricted immune-checkpoint modulation, itaconate-centered metabolic reprogramming, calibrated inflammasome targeting, investigation of IL-22-mediated epithelial protection, and controlled extracellular-matrix remodeling to improve antimicrobial delivery. Translation should follow a tiered strategy rather than assuming universal deployment of advanced technologies. Transcriptomic endotyping, spatial profiling, and PET-CT may be particularly valuable for patient enrichment, mechanistic phenotyping, and pharmacodynamic assessment in early-phase trials and specialized referral centers, whereas their limited accessibility in many high-burden and resource-constrained settings currently precludes their use as routine prerequisites for HDT implementation. Conventional microbiologic outcomes should also be complemented by mechanistically informative endpoints, including time-to-positivity, radiographic cavity closure, lesion resolution, and restoration of tissue-resident memory T-cell responses.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusions: &lt;/strong&gt;The next phase of TB therapeutics may depend not only on developing additional antimicrobials but also on dismantling the host-derived niches that sustain Mtb persistence. Treating the granu","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-28"},"PeriodicalIF":2.3,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792582","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":"Myokines, Microbiota, and Neuroinflammation: Physical Activity Modulates the Gut-Brain Axis.","authors":"Yahui Yang, Ye Yang, Yingjuan Tang, Weilin Yang","doi":"10.1080/08820139.2026.2689670","DOIUrl":"https://doi.org/10.1080/08820139.2026.2689670","url":null,"abstract":"<p><strong>Background: </strong>Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis are increasingly recognized as disorders influenced not only by intrinsic neural pathology but also by systemic physiological networks, including the gut-brain axis. Emerging evidence highlights physical activity as a potent modulator of this bidirectional communication system, with muscle-derived signals particularly myokines, metabolites, and extracellular vesicles playing a central role.</p><p><strong>Methods: </strong>This narrative review synthesizes current knowledge on how exercise-induced molecular mediators influence gut microbiota composition, intestinal barrier integrity, immune signaling, and neuroinflammatory pathways. Findings were integrated across the disciplines of neuroscience, microbiology, and exercise physiology to evaluate mechanistic links between muscle-secreted factors and gut-mediated responses.</p><p><strong>Results: </strong>Mechanistic links exist between muscle-secreted factors such as irisin, cathepsin B, BDNF-inducing pathways, and lactate with microbial metabolites including short-chain fatty acids. These interacting pathways demonstrate a combined impact on neuroprotection, synaptic plasticity, and the modulation of disease progression in neurodegenerative conditions.</p><p><strong>Conclusion: </strong>Physical activity represents a promising non-pharmacological strategy for modulating the gut-brain axis in neurodegenerative conditions. Understanding the interplay between muscle-derived signals and gut-mediated pathways may open new avenues for targeted interventions aimed at slowing or preventing neurodegenerative decline.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-28"},"PeriodicalIF":2.3,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706376","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":"KEAP1-Nrf2 Signaling in Chronic Inflammatory Disorders: Integrating Redox Biology, Quantitative Evidence, and Precision Therapeutics.","authors":"Abdul Shadab","doi":"10.1080/08820139.2026.2714418","DOIUrl":"https://doi.org/10.1080/08820139.2026.2714418","url":null,"abstract":"<p><strong>Background: </strong>Chronic inflammatory disorders represent a major global health burden characterized by persistent immune activation, oxidative stress, and progressive tissue dysfunction. Dysregulated redox signaling has positioned the Kelch-like ECH-associated protein 1 (KEAP1)-nuclear factor erythroid 2-related factor 2 (Nrf2) axis as an emerging therapeutic target.</p><p><strong>Methods: </strong>This review critically examines the mechanistic architecture and context-dependent regulation of KEAP1-Nrf2 signaling across chronic inflammatory disorders, integrating disease-specific evidence, signaling crosstalk, quantitative preclinical findings, therapeutic modulators, nanoenabled delivery systems, clinical evidence, patent trends, and artificial intelligence-assisted drug discovery strategies.</p><p><strong>Results: </strong>KEAP1-Nrf2 signaling extends beyond antioxidant defense to regulate immunometabolic homeostasis, mitochondrial function, inflammatory signaling, and cellular stress adaptation. Crosstalk with NF-κB, MAPK, PI3K/Akt, and inflammasome-associated pathways contributes to disease-specific inflammatory responses. Preclinical evidence supports natural and synthetic Nrf2 modulators, while nanotechnology-based approaches may improve delivery and tissue specificity. However, dose optimization, bioavailability, off-target effects, long-term safety, and patient heterogeneity remain important translational challenges.</p><p><strong>Conclusion: </strong>KEAP1-Nrf2 represents a context-dependent therapeutic axis with substantial potential across chronic inflammatory diseases. Integrating quantitative evidence, precision delivery, biomarker-guided approaches, and computational strategies may facilitate clinical translation while addressing risks associated with sustained pathway activation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-69"},"PeriodicalIF":2.3,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148706316","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 Transcriptional States of Human Leukocyte Antigen DR Positive CD4 Positive T Cells Linked to Genetic Susceptibility of Gastric Cancer.","authors":"Yicun Song, Haoran Zhu, Cong Qiao, Yueying Wang","doi":"10.1080/08820139.2026.2708205","DOIUrl":"https://doi.org/10.1080/08820139.2026.2708205","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) involves complex immune-metabolic crosstalk, but MR-prioritized immunophenotypes and mediating metabolites remain unclear.</p><p><strong>Methods: </strong>Two-sample Mendelian randomization (MR) was performed using GWAS summary data for 731 immunophenotypes, 1,400 circulating metabolites, and GC (218,792 European participants). Instruments were selected at <i>p</i> < 1 × 10^-5, LD-clumped (r² < 0.001, 10,000 kb), and filtered for strength (F > 10). IVW served as the primary estimator, with sensitivity and reverse MR analyses. Two-step MR explored metabolite-mediated pathways. Single-cell RNA-seq from 56 samples across three sources was integrated to resolve HLA-DR⁺ CD4⁺ T-cell transcriptional states, evaluate GC genetic-risk enrichment via scDRS, and infer cell-cell communication using CellChat.</p><p><strong>Results: </strong>Twenty-six immunophenotypes showed candidate associations with GC. HLA-DR expression on HLA-DR⁺ CD4⁺ T cells was inversely associated with GC risk (OR = 0.761, 95% CI 0.634-0.912, FDR q = 0.0393). Reverse MR was not FDR-significant, and MR-Egger indicated no directional pleiotropy. Candidate mediation involved bilirubin degradation product C17H18N2O4(2). Single-cell analysis identified five HLA-DR⁺ CD4⁺ T-cell subsets; T1 and T5 showed relatively higher GC genetic-susceptibility enrichment, with T5 exhibiting low CytoTRACE scores. These subsets were linked to immune activation and chemokine signaling. The exploratory TIGIT-NECTIN2 signal was not robustly retained after CellChat sensitivity filtering.</p><p><strong>Conclusion: </strong>This study suggests a potential inverse association between HLA-DR⁺ CD4⁺ T-cell immunophenotypes and GC risk, with bilirubin-related metabolites as a candidate mediating pathway. Subsets T1/T5 provide candidate directions for future GC immune-prevention research.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-32"},"PeriodicalIF":2.3,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677330","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":"Numb Mediates IL-1β/TGF-β1-Driven Inflammation-Fibrosis Coupling in Idiopathic Pulmonary Fibrosis.","authors":"Debin Zhuo, Shanzuan Wang, Juan Lin, Guohuan Chen","doi":"10.1080/08820139.2026.2693028","DOIUrl":"https://doi.org/10.1080/08820139.2026.2693028","url":null,"abstract":"<p><strong>Background: </strong>In idiopathic pulmonary fibrosis (IPF), inflammatory signaling and fibrotic remodeling often coexist, yet the mechanism linking these processes remains unclear. Numb, a cell fate determinant protein, has been implicated in tissue remodeling but its role in inflammation - fibrosis coupling is not well defined.</p><p><strong>Methods: </strong>Public transcriptomic datasets were analyzed to assess NUMB expression patterns and associated pathways. A bleomycin (BLM)-induced mouse model was used for in vivo validation. In vitro, MRC-5 fibroblasts were stimulated with IL-1β and TGF-β1, alone or in combination, followed by Numb siRNA intervention. Cell viability, migration, cytokine secretion, and fibrosis-related protein expression were evaluated.</p><p><strong>Results: </strong>Transcriptomic analysis showed a non-significant but consistent upward trend of NUMB in IPF tissues (<i>p</i> = .18), with pathway-level enrichment in inflammatory and extracellular matrix processes. In BLM-treated mice, IL-1β and TGF-β1 levels were significantly increased (both <i>p</i> < .001), accompanied by upregulation of Numb (<i>p</i> < .05), α-SMA, and Collagen I (both <i>p</i> < .001). In vitro, IL-1β and TGF-β1 synergistically enhanced cell viability and migration (both <i>p</i> < .001), as well as protein expression (<i>p</i> < .001). Numb silencing reduced cytokine secretion (<i>p</i> < .001), cell activation (<i>p</i> < .05-0.001), and fibrosis-related protein expression (<i>p</i> < .001).</p><p><strong>Conclusion: </strong>Numb participates in coordinating inflammatory and fibrotic responses in IPF and may act as a regulatory mediator in inflammation - fibrosis coupling.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-18"},"PeriodicalIF":2.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669126","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":"γδ T Cells as a Platform for Immunotherapy: From Biological Principles to Clinical Translation.","authors":"Junjie Ni, Chao Xiong, Xian Wu, Zijun Yuan, Xingyue Wang, Yu Chen, Xu Wu, Mingxing Li, Fukuan Du, Yueshui Zhao, Zhuo Chen, Jing Shen, Xi He, Zhangang Xiao","doi":"10.1080/08820139.2026.2711303","DOIUrl":"https://doi.org/10.1080/08820139.2026.2711303","url":null,"abstract":"<p><p><b>Background:</b> γδ T cells are emerging as a promising immunotherapy platform because they combine rapid innate-like effector activity with adaptive immune features and recognize stress-associated signals in a largely MHC-independent manner. Their clinical utility, however, is constrained by pronounced heterogeneity in subset composition, tissue localization, and functional state.<b>Objective:</b> This review aims to summarize the biological principles governing γδ T-cell development, classification, and antigen recognition and to examine how their context-dependent functions inform therapeutic design.<b>Methods:</b> We integrated current evidence on γδ T-cell biology across cancer, infection, and autoimmunity and evaluated the major translational strategies currently being developed.<b>Results:</b> Current strategies include in vivo activation, adoptive transfer, combination regimens, engineered γδ T-cell products, and cell-free approaches such as γδ T-cell-derived extracellular vesicles. However, clinical translation remains limited by product heterogeneity, insufficient expansion and persistence, and incomplete mechanistic resolution.<b>Conclusion:</b> Future development should prioritize mechanism-guided engineering, biomarker-informed development, and better-designed clinical studies.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-29"},"PeriodicalIF":2.3,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148669199","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":"Precision Warfare in Solid Tumors: Molecular Mechanisms and Emerging Frontiers of Antibody-Drug Conjugates.","authors":"Hanandha Putra Luqmana, Ami Ashariati, Merlyna Savitri, Betty Rachma, Henry Sutanto","doi":"10.1080/08820139.2026.2713194","DOIUrl":"https://doi.org/10.1080/08820139.2026.2713194","url":null,"abstract":"<p><p><b>Background:</b> Antibody-drug conjugates (ADCs) have transformed the treatment of solid tumors by combining the tumor specificity of monoclonal antibodies with highly potent cytotoxic payloads. Advances in ADC engineering have expanded their clinical applications while addressing limitations of conventional chemotherapy and targeted therapies.<b>Methods:</b> We conducted a comprehensive narrative review of the molecular mechanisms, structural design, resistance pathways, clinical translation, and emerging engineering strategies of ADCs in solid tumors, integrating evidence from preclinical and clinical studies.<b>Results:</b> ADC efficacy is governed by antigen selection, linker chemistry, payload characteristics, and drug-to-antibody ratio, which collectively influence pharmacokinetics, tumor penetration, intracellular trafficking, and payload release. Key mechanisms include receptor-mediated internalization, lysosomal processing, bystander killing, immune modulation, and interactions with the tumor microenvironment. Major resistance mechanisms comprise antigen heterogeneity, impaired intracellular trafficking, drug efflux, adaptive DNA repair, and stromal barriers. Emerging innovations-including site-specific conjugation, bispecific and conditionally activated ADCs, novel payloads, biomarker-guided patient selection, and rational combination therapies-are enhancing therapeutic efficacy and expanding targetable tumors.<b>Conclusion:</b> Continued advances in molecular engineering and precision biomarker strategies are redefining ADCs as versatile platforms for precision oncology and may enable broader, potentially tumor-agnostic, applications in solid tumors.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1-39"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653685","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":"Research Progress on Non-Coding RNA-Mediated Macrophage Polarization in Chronic Obstructive Pulmonary Disease.","authors":"Ai Ma, Xiaofeng Li, Xiaoli Zeng, Xiaoju Liu","doi":"10.1080/08820139.2026.2668694","DOIUrl":"10.1080/08820139.2026.2668694","url":null,"abstract":"<p><strong>Background: </strong>Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disorder characterized by remarkable heterogeneity. Its pathogenesis involves inflammatory responses, oxidative stress, protease-antiprotease imbalance, and immune dysregulation. Recent studies have demonstrated that macrophages, as key components of the innate immune system, play a pivotal regulatory role in COPD pathogenesis through phenotypic polarization. Non-coding RNAs (ncRNAs) serve as critical regulatory factors that can finely orchestrate macrophage polarization and functional states through diverse mechanisms, including post-transcriptional gene silencing, chromatin remodeling, and competing endogenous RNA (ceRNA) networks, thereby influencing the inflammatory processes and pathological progression of COPD.</p><p><strong>Methods and results: </strong>This review comprehensively searched for domestic and international literature on macrophage polarization, ncRNAs, and COPD, and analyzed and summarized the relevant content. This article mainly discussed macrophage polarization in COPD, analyzed the regulatory roles of different ncRNA subtypes in macrophage M1/M2 polarization, the molecular mechanisms by which ncRNAs participate in the development and progression of COPD through regulating macrophage polarization, and evaluated the value of ncRNAs targeting macrophage polarization as potential biomarkers for COPD, as well as the prospects and challenges of ncRNA-targeted therapy for COPD.</p><p><strong>Conclusion: </strong>This review summarizes the current research progress on ncRNAs regulating macrophage polarization in COPD, with the aim of deepening the understanding of the underlying molecular mechanisms, identifying novel biomarkers for disease diagnosis, subtyping, and prognostic assessment, reviewing ncRNA-targeted therapeutic strategies, exploring precise regulation centered on the ncRNA-macrophage polarization axis, and providing new insights for personalized diagnosis and treatment of COPD.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1264-1295"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147836963","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 Clinical Efficacy and Safety of Efgartigimod in the Treatment of Autoimmune Encephalitis.","authors":"Jin Qin, Jiewen Zhang","doi":"10.1080/08820139.2026.2665257","DOIUrl":"10.1080/08820139.2026.2665257","url":null,"abstract":"<p><strong>Objective: </strong>Efgartigimod, an innovative human IgG Fc receptor antagonist, clears pathogenic IgG autoantibodies. However, its efficacy and safety in autoimmune encephalitis (AE) remain undefined.</p><p><strong>Methods: </strong>We retrospectively analyzed the modified Rankin Scale (mRS) scores, Clinical Assessment Scale for Autoimmune Encephalitis (CASE) scores, immunological parameters, and routine clinical laboratory data from AE patients treated with efgartigimod.</p><p><strong>Results: </strong>The study included 15 AE patients who received efgartigimod. After the initial 4-week treatment period, a clinically meaningful improvement was observed in mRS scores [median: 4 (IQR 3, 5) vs. 2 (IQR 1, 2)]and CASE scores [median: 13 (IQR 7, 16) vs. 2 (IQR 1, 3)] (<i>p</i> < .001). Subgroup analyses further suggested a trend of clinical improvement in AE patients with neuronal surface autoantibodies (NSAab) (<i>p</i> < .01). Alongside clinical improvement, serum IgG levels decreased after the first infusion and continued to decline with subsequent treatments (<i>p</i> < .05). No serious adverse events were reported. Other immune markers and clinical laboratory parameters showed no observable changes (<i>p</i> > .05).</p><p><strong>Conclusions: </strong>In this small retrospective cohort, efgartigimod was associated with clinical improvement and selectively reduced IgG levels with an acceptable safety profile. However, no causal relationship was established between IgG reduction and clinical response. These findings need further validation.</p>","PeriodicalId":13387,"journal":{"name":"Immunological Investigations","volume":" ","pages":"1194-1208"},"PeriodicalIF":2.3,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972334","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}