Junyun Huang

[This corrects the article DOI: 10.3389/fimmu.2026.1747972.].

Background: This study aimed to explore DDX17 protein expression as a diagnostic biomarker of hepatocellular carcinoma (HCC) and its roles in the occurrence and development of HCC. Methods: The proteomics sequencing method was applied to study nine samples of exosomes separated from HCC tissues and corresponding normal non-cancerous tissues. We also performed nanoflow cytometry analysis of DDX17 expression in serum-derived exosomes from 102 HCC patients, 58 persons with liver cirrhosis (LC), and 80 healthy donors (HDs). The feasibility of DDX17 as a diagnostic and prognostic biomarker was evaluated using receiver operating characteristic (ROC) curves. The effects of HCC-derived exosomal DDX17 on LX-2 cell proliferation, migration, and epithelial–mesenchymal transition (EMT) were evaluated through cell proliferation, colony formation, wound healing, transwell migration, and western blotting assays. Results: We found that exosomes produced by HCC cells had much higher levels of DDX17 than those produced by the adjacent non-cancerous tissues. ROC analysis showed that exosomal DDX17 has a strong ability to distinguish HCC with both high sensitivity and high specificity. If the exosomal DDX17 result is negative, then we expect it to be a new kind of diagnostic biomarker. Moreover, we observed that DDX17-positive exosome subtypes isolated from the HepG2 cell line increased cell proliferation, migration, invasion, and EMT in the LX-2 cell line. Conclusion: DDX17-positive exosomes are potential diagnostic biomarkers of HCC and are expected to promote tumor growth, migration, invasion, and EMT.

Parkinson’s disease (PD) is the second most common neurodegenerative disorder, and its rising incidence poses a growing burden on productivity and healthcare systems, particularly in the context of global population aging. Despite substantial advances in research, the pathogenesis of PD remains incompletely understood, and no curative or effective preventive therapies are currently available. Emerging evidence suggests a potential link between fatty acid (FA) metabolism and PD pathogenesis, positioning the modulation of FA metabolic pathways as a promising therapeutic strategy. This review examines the interplay between FA metabolism and key pathological processes, including oxidative stress, neuroinflammation, and the abnormal aggregation of alpha-synuclein, within the context of PD. By integrating these perspectives, the article aims to advance understanding of disease mechanisms and identify novel opportunities for prevention, early diagnosis, and targeted treatment.

Tuberculosis (TB) is one of the most common infectious diseases caused by Mycobacterium tuberculosis (M.tb). The emergence of multidrug-resistant strains, HIV infection, and poor efficacy of the BCG vaccine have made TB epidemics difficult to control. Natural killer (NK) cells are an important component of the body’s innate immunity, playing a role not only in the early stages of M.tb infection but also in activating adaptive immune cells to inhibit M.tb proliferation. Recent studies have increasingly revealed significant changes in the number, subsets, and functions of NK cells as TB progresses, with NK cells primarily exhibiting signs of depletion, suggesting a close correlation between NK cell changes and TB progression. Therefore, this article outlines the main changes in NK cells in clinical cohort studies, discusses potential mechanisms of their depletion, and introduces the functions of NK cells, as well as the methods and strategies they use to recognize and kill Mycobacterium tuberculosis. This can contribute to a better understanding of the role and manifestation of NK cells in TB immunity and provide a more comprehensive perspective for NK cell-based TB treatment strategies.

Current dual base editors and hypermutators exhibit limited types of base conversion and constrained mutational diversity. To address this challenge, we engineer a compact dual base editor “A&GBE” by fusing a deaminase and glycosylase with nickase Cas9 (nCas9) to enable concurrent adenine and cytosine editing. Furthermore, we develop quadruple base mutating modules (QBMM) by fusing nickase or dead Cas9 with engineered thymine-DNA glycosylase (TDG), N-methylpurine DNA glycosylase (MPG) and TadA8e, together with MS2-MCP system recruited activation-induced cytidine deaminase (AID). This QBMM enables simultaneous mutation of all four types of nucleotide bases (A, T, G, C) within an approximately 100 base pair (bp) sequence surrounding the gRNA target site. This platform generates hyper diverse multi-nucleotide variants, establishing a powerful tool for accelerated protein evolution, functional genomics, and disease modeling.

Introduction: Natural killer (NK) cells contribute to immunity against Mycobacterium tuberculosis ( Mtb ), yet their granzyme expression and subset distribution in TB remain poorly defined. Methods: NK cell subsets and the expression of granzymes (GZMA, GZMB, and GZMK) and CCR5 were analyzed by multiparametric flow cytometry in peripheral blood from healthy controls, individuals with latent TB infection, active TB patients, and treated TB patients, as well as in paired pleural fluid samples. Results: In peripheral blood from active TB patients, NK cells exhibited reduced co-expression of GZMA, GZMB, and GZMK alongside decreased subset frequencies and absolute counts, a defect restored after treatment. In contrast, pleural fluid NK cells exhibited a distinct signature characterized by elevated GZMK but reduced GZMA and GZMB. This pattern was attributable to the relative enrichment of CD56 ^bright NK cells, which are inherently high in GZMK. We also identified a CCR5 ^bright NK cell subset, phenotypically resembling CD56 ^bright NK cells with high GZMK and low GZMA/GZMB expression, that was selectively expanded in peripheral blood of TB patients and enriched in pleural effusions. This subset was inducible by in vitro Mtb stimulation of healthy PBMCs. Discussion: These findings reveal granzyme remodeling and altered distribution of GZMK ⁺ CD56 ^bright NK cells associated with CCR5 ^bright expression in TB, suggesting their potential involvement in tissue-specific NK responses.

Neurodegenerative diseases are a group of chronic diseases characterized by a gradual loss of neurons that worsens over time and dysfunction. These diseases are extremely harmful, not only affecting the physical health of the patients, but also having a serious impact on their quality of life. They mainly include Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), Amyotrophic lateral sclerosis (ALS), etc. Their pathogenesis is complex, and it is difficult for the existing treatments to effectively slow down the progression of the disease. In recent years, Mesenchymal Stem Cells (MSCs) have received widespread attention for their anti-inflammatory, immunomodulatory and neuroprotective properties. In this context, MSC-derived Extracellular Vesicles (MSC-EVs) have demonstrated unique therapeutic potential as a cell-free therapeutic strategy. MSC-EVs are rich in bioactive substances such as proteins, lipids, mRNAs and miRNAs, which can pass through the blood-brain barrier and be targeted to the diseased area to regulate neuronal survival, synaptic plasticity and neuroinflammatory responses. In addition, compared with stem cell therapy, MSC-EVs have the advantages of low immunogenicity, easy storage and transportation, and avoiding ethical controversies. However, their clinical application still faces challenges: standardized isolation and purification techniques have not been unified, vesicle loading efficiency and targeting need to be further optimized, and long-term safety needs to be systematically evaluated. This review focuses on the role of MSC-EVs in the development of neurological diseases and explores their possible dual roles, both favorable and unfavorable, in the context of neurological diseases. In addition, this review provides a review of current studies on EVs as potential biomarkers for the diagnosis and treatment of neurodegenerative diseases and provides a comprehensive review of the prospects and challenges of MSC-EVs in clinical applications.

Cryptococcus neoformans, a prominent opportunistic pathogen, is equipped with unique mechanisms to evade host immune defenses, notably through its capsule and the secretion of extracellular vesicles (EVs). Despite significant understanding of its pathogenesis, the precise role of EVs in virulence and their molecular components remain underexplored. This review synthesizes current research on the virulence factors encapsulated within EVs of Cryptococcus, highlighting their contribution to fungal survival and pathogenicity. By analyzing the biochemical composition of these vesicles, we found the presence of enzymes (e.g., Urease, laccase), toxins (e.g. Melanin), and genes (e.g. Ssa1) associated with pathogenicity factors. Furthermore, we discuss the implications of these findings for developing therapeutic interventions. This work advances the field by providing a comprehensive overview of EV-mediated mechanisms in Cryptococcus, offering new insights into potential targets for antifungal strategies.

Mesenchymal stem cells (MSCs) are currently being used in clinical trials for the treatment of a wide range of diseases and have a wide range of applications in the fields of tissue engineering and regeneration. Exosomes are extracellular vesicles containing a variety of components such as proteins, nucleic acids and lipids, which are widely present in biological fluids and have the functions of participating in intercellular information transfer, immune response and tissue repair, and can also be used as carriers to target and deliver tumors to improve therapeutic effects. Mesenchymal stem cell-derived Exosomes (MSC-Exos), which have the advantages of low immunogenicity and high tumor homing ability, have attracted much attention in targeted drug delivery. Here, we review the current knowledge on the involvement of MSC-Exos in tumor progression and their potential as drug delivery systems in targeted therapies. It also discusses the advantages and prospects of MSC-Exos as a drug carrier and the challenges that still need to be overcome.