ArticleInternational journal of molecular sciences2025
Aflatoxin B1 Exposure Suppresses the Migration of Dendritic Cells by Reshaping the Cytoskeleton.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Targeting Mycotoxin Toxicity: From Molecular Mechanisms to Nutritional Interventions.Veterinary sciences · 2026Review
- Protective effects of commercial artichoke (Cynara scolymus L.) leaf powder against aflatoxin B1-induced reproductive toxicity in male rats.Mycotoxin research · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Exposure to Aflatoxin B1 (AFB1) is considered a significant risk factor for human diseases, including the immune function impairment of immune cells. Dendritic cells (DCs), as essential antigen-presenting cells, play a pivotal role in bridging innate and adaptive immunity. However, the impact of AFB1 exposure on DCs has not been fully elucidated. In this study, we investigated the effects of AFB1 exposure on the migration ability of DCs and its underlying action model. Initially, we observed that AFB1 exposure inhibited the survival of DCs and altered their cellular morphology. Further investigation revealed that AFB1 promotes cell adhesion and inhibits DC migration by modulating the expression of cell adhesion molecules. Additionally, our findings indicated that cytoskeletal remodeling plays a crucial role in these processes. Experimental techniques such as immunofluorescence and RNA sequencing confirmed that AFB1 exposure regulates the expression of cytoskeleton-related genes. Moreover, we found that the perturbation of the gene expression profile through AFB1 exposure is associated with cell communication. Collectively, our study findings demonstrate that AFB1 can disrupt the expression of cytoskeleton- and adhesion-related molecules in DCs, thereby altering cell morphology and migration. These insights could provide new perspectives for further understanding the immunosuppressive effects of AFB1 and developing therapeutic strategies for diseases associated with AFB1 exposure.
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