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Autoimmune diseases refer to a group of conditions where the immune system produces an immune response against self-antigens, resulting in tissue damage. These diseases have profound impacts on the health of patients. In recent years, with the rapid development in the field of biomedicine, engineered exosomes have emerged as a noteworthy class of biogenic nanoparticles. By precisely manipulating the cargo and surface markers of exosomes, engineered exosomes have gained enhanced anti-inflammatory, immunomodulatory, and tissue reparative abilities, providing new prospects for the treatment of autoimmune diseases. Engineered exosomes not only facilitate the efficient delivery of bioactive molecules including nucleic acids, proteins, and cytokines, but also possess the capability to modulate immune cell functions, suppress inflammation, and restore immune homeostasis. This review mainly focuses on the applications of engineered exosomes in several typical autoimmune diseases. Additionally, this article comprehensively summarizes the current approaches for modification and engineering of exosomes and outlines their prospects in clinical applications. In conclusion, engineered exosomes, as an innovative therapeutic approach, hold promise for the management of autoimmune diseases. However, while significant progress has been made, further rigorous research is still needed to address the challenges that engineered exosomes may encounter in the therapeutic intervention process, in order to facilitate their successful translation into clinical practice and ultimately benefit a broader population of patients.

The aim of this study was to investigate lymphocyte subsets, especially natural killer (NK) cells, in patients with systemic sclerosis (SSc) and evaluate the diagnostic value of NK cells in secondary pulmonary arterial hypertension (PAH). A total of 115 SSc patients and 100 age- and sex-matched health controls (HCs) were enrolled in this study. Flow cytometry was employed to quantify NK cells, while the association between NK cells and disease activity as well as PAH was investigated to further elucidate its diagnostic potential. The absolute count of NK (CD3-CD56+) cells significantly decreased in SSc patients. There was a negative correlation between the mRSS score and the injury index. The levels of cytokine exhibited significant elevation among SSc patients. Conversely, SSc-PAH patients demonstrated significantly elevated levels of CRP, UA, and BNP. Additionally, there was a significant reduction in the absolute level of NK cells. ROC curve analysis revealed that the optimal cut-off point for NK cells was 185 cells/µL, while for BNP it was 70.50 pg/mL and for UA it was 323.00 µmol/L. Our study revealed a significant inverse correlation between peripheral blood NK cell levels and the incidence of complicated PAH in patients with SSc.

Introduction Caveolins (Cav) include Cav‐1, Cav‐2, and Cav‐3, with Cav‐1 being the most studied due to its prominent role as a major component of plasma membrane caveolae. Cav‐1 is involved in a wide range of cellular functions and plays a key role in regulating signaling pathways related to immune responses and inflammation. Recently, research on Cav‐1 in autoimmune diseases (AIDs) has garnered significant interest. Methods This paper provides an overview of the research on Cav‐1's involvement in AIDs, including rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, anti‐neutrophil cytoplasmic antibody‐associated vasculitis, systemic sclerosis, connective tissue disease‐associated interstitial lung disease, autoimmune disorders of the nervous system, autoimmune uveitis, autoimmune thyroid disease, and autoimmune myocarditis. Results Cav‐1 plays a critical role in various AIDs, acting as a key protein in inflammatory and immune cells. It regulates multiple signaling processes by controlling the translocation of signaling molecules and modulating various pathways. Cav‐1 is increasingly recognized as a biomarker in certain AIDs and may become pivotal in treating these diseases in the future. Conclusion Cav‐1 is a crucial player in the pathogenesis of many AIDs and has the potential to serve as both a diagnostic marker and a therapeutic target for these diseases. As research into Cav‐1 deepens, it may offer new insights into the diagnosis, treatment, and drug sensitivity of AIDs, emerging as a promising target for future therapeutic strategies.

BackgroundMalignant neoplasms are a well-recognized global public health concern, with significant impacts on human health and quality of life. The interplay between tumors and autoimmune rheumatic diseases is complex, and the resulting tumor-associated rheumatic diseases represent a rare and intricate group of conditions that occur in the context of malignant tumors. In addition, various rheumatic diseases can arise as a consequence of oncology treatment. These diseases present with intricate clinical manifestations and pathological features, often rendering them challenging to diagnose and impacting patients' quality of life. Despite this, they have yet to be fully recognized.MethodsThis article presents a literature review of published original articles and review articles concerning paraneoplastic rheumatic syndromes and rheumatic diseases associated with cancer treatment. We conducted a comprehensive literature search in PubMed, Web of Science and Google Scholar databases, excluding duplicated and irrelevant studies. In cases of duplicated research, we selected articles with higher impact factors for the review.ResultsThis review focuses on the clinical features, diagnosis, and treatment of paraneoplastic rheumatic diseases, as well as the pathogenesis of these diseases. Additionally, we summarize the autoimmune rheumatic diseases associated with cancer treatment. Ultimately, the goal of this review is to enhance recognition and improve the management of autoimmune rheumatic diseases related to tumors.

The intestinal barrier integrity is essential for the absorption of nutrients and health in humans and animals. Dysfunction of the mucosal barrier is associated with increased gut permeability and development of multiple gastrointestinal diseases. Recent studies highlighted a critical role for glutamine, which had been traditionally considered as a nutritionally non-essential amino acid, in activating the mammalian target of rapamycin cell signaling in enterocytes. In addition, glutamine has been reported to enhance intestinal and whole-body growth, to promote enterocyte proliferation and survival, and to regulate intestinal barrier function in injury, infection, weaning stress, and other catabolic conditions. Mechanistically, these effects were mediated by maintaining the intracellular redox status and regulating expression of genes associated with various signaling pathways. Furthermore, glutamine stimulates growth of the small intestinal mucosa in young animals and also enhances ion transport by the gut in neonates and adults. Growing evidence supports the notion that glutamine is a nutritionally essential amino acid for neonates and a conditionally essential amino acid for adults. Thus, as a functional amino acid with multiple key physiological roles, glutamine holds great promise in protecting the gut from atrophy and injury under various stress conditions in mammals and other animals.

Bivalve molluscs are descendants of an early-Cambrian lineage superbly adapted to benthic filter feeding. Adaptations in form and behavior are well recognized, but the underlying molecular mechanisms are largely unknown. Here, we investigate the genome, various transcriptomes, and proteomes of the scallop Chlamys farreri , a semi-sessile bivalve with well-developed adductor muscle, sophisticated eyes, and remarkable neurotoxin resistance. The scallop’s large striated muscle is energy-dynamic but not fully differentiated from smooth muscle. Its eyes are supported by highly diverse, intronless opsins expanded by retroposition for broadened spectral sensitivity. Rapid byssal secretion is enabled by a specialized foot and multiple proteins including expanded tyrosinases. The scallop uses hepatopancreas to accumulate neurotoxins and kidney to transform to high-toxicity forms through expanded sulfotransferases, probably as deterrence against predation, while it achieves neurotoxin resistance through point mutations in sodium channels. These findings suggest that expansion and mutation of those genes may have profound effects on scallop’s phenotype and adaptation. Bivalve molluscs have evolved various characteristics to adapt to benthic filter-feeding. Here, Li et al investigate the genome, transcriptomes and proteomes of scallop Chlamys farreri , revealing evidences of molecular adaptations to semi-sessile life and neurotoxins.

Melatonin is a well-known anti-inflammatory and antioxidant molecule, which plays a crucial role in various physiological functions. In this study, mice received a single dose of 15 Gy radiation delivered to the lungs and daily intraperitoneal administration of melatonin. After 7 days, mice were processed to harvest either bronchoalveolar lavage fluid for cytokine assays or lungs for flow cytometry and histopathological studies. Herein, we showed that melatonin markedly alleviated the oxidative stress and injury, especially suppressing the infiltration of macrophages (CD11b+CD11c−) and neutrophils (CD11b+Ly6G+) to the irradiated lungs. Moreover, in the irradiated RAW 264.7 cells, melatonin blocked the NLRP3 inflammasome activation accompanied with the inhibition of the IL-1β release and caspase-1 activity. However, melatonin restored the downregulated miR-30e levels. Quantitative PCR analysis of miR-30e and NLRP3 indicated the negative correlation between them. Notably, immunofluorescence staining showed that overexpression of miR-30e dramatically diminished the increased NLRP3 expression. Luciferase reporter assay confirmed that NLRP3 was a target gene of miR-30e. Western blotting revealed that transfection with miR-30e mimics markedly reduced the expressions of NLRP3 and cleaved caspase-1, whereas this phenomenon was reversed by the miR-30e inhibitor. Consistent with this, the beneficial effect of melatonin under irradiated exposure was blunted in cells transfected with anti-miR-30e. Collectively, our results demonstrate that the NLRP3 inflammasome contributed to the pathogenesis of radiation-induced lung injury. Meanwhile, melatonin exerted its protective effect through negatively regulating the NLRP3 inflammasome in macrophages. The melatonin-mediated miR-30e/NLRP3 signaling may provide novel therapeutic targets for radiation-induced injury.

Hydrogels are crucial for soft bioelectronics in long-term health monitoring; however, reconciling skin comfort with environmental resilience remains a major challenge. We present a 392 nm-thick organohydrogel nanofilm electrode that mimics skin deformation, offers high gas/water vapor/sweat permeability and heat transfer, and remains functional under various extreme conditions. The electrode comprises a genipin-crosslinked gelatin matrix, reinforced by polyurethane nanomeshes and plasticized with a glycerol/sodium chloride/tannic acid electrolyte. It achieves ultralow flexural rigidity (8.7 × 10 −11 nN·m), high stretchability (166.3% strain), toughness (3.0 MJ m −3 ), adhesion (365.8 µJ cm −2 ), and durability (1000 cycles at 100% strain). Solvent replacement strategies suppress ice formation and evaporation, preserving its physical and electrical performance under extreme conditions (−80–150 °C, 2% relative humidity, vacuum) and 200-day ambient storage. The organohydrogel nanofilm electrodes record stable electrocardiograms for 9 consecutive days with superior resistance to motion and sweat artifacts, offering a resilient platform for skin-integrated bioelectronics. Hydrogels can be integrated into skin bioelectronics, though balancing stability, mechanical properties, and breathability remains challenging. Here the authors design a crosslinked organohydrogel using a solvent replacement strategy integrated into on-skin sensors.

In online teaching scenarios, automatic assessment of student engagement suffers from limited real-time capability, high computational cost, and redundant information in long-duration videos. To address these challenges, a student engagement recognition model driven by prediction error–based memory updating (DMDN) is proposed. A multi-stage framework with feature decoupling is adopted. A behavior dynamics branch is used to extract coarse-grained behavioral features. A facial attention branch is used to extract fine-grained facial representations. Semantic interference during heterogeneous visual feature modeling is thus avoided. Furthermore, a dynamic memory updating module based on prediction error is introduced. The deviation between current observations and historical memory is characterized. The memory update strength is adaptively adjusted. Selective encoding of key behavioral segments is achieved. Interference from redundant temporal information is effectively suppressed. The model parameters and deployment scheme are revised as follows. A two-stage deployment strategy is adopted, in which backbone features are extracted and cached offline, decoupling heavy feature extraction from online inference. Only a lightweight inference backend with 3.18M trainable parameters is executed during real-time prediction. Experimental results on the DAiSEE dataset demonstrate that a Top-1 accuracy of 64.65% is achieved, validating the effectiveness of the proposed method under strict computational constraints. This design demonstrates its potential in resource-constrained scenarios. Ablation studies further verify the effectiveness of the feature decoupling structure and the dynamic memory update mechanism in improving performance.

The genus Fusobacterium encompasses significant pathogens implicated in diseases spanning from infections to cancer. However, taxonomic ambiguities persist within the genus, particularly concerning Fusobacterium nucleatum ( sensu lato ). Through genus-wide average nucleotide identity (ANI) and phylogenetic analyses of 540 Fusobacterium genomes, we identify an ANI gap (93.38%−93.89%) for species delineation, leading to comprehensive taxonomic revisions that resolve these ambiguities. We further establish gyrB and rpoB as high-resolution taxonomic markers with phylogenies consistently supporting the revised taxonomy. Leveraging these markers, we develop B&B, a general strategy for precise species identification without whole-genome sequencing, and validate its accuracy in clinically relevant strains. Integrating the revised taxonomy with genomic/metagenomic toolkits demonstrate broad utilities, reinterpreting key colorectal cancer-associated species. This work establishes a unified taxonomic framework and enables standardised species classification for Fusobacterium isolates and microbiomes, highlighting the genetic divergence among Fusobacterium species and providing the taxonomic precision essential for advancing Fusobacterium -related research. Bacteria of the genus Fusobacterium are associated with diverse diseases, but taxonomic ambiguities complicate species-level identification. Here, the authors describe practical methods for Fusobacterium species identification, which allows a reinterpretation of disease associations.