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.

Fumonisin B1 (FB1) is one of the most toxic mycotoxins and is harmful to humans and animals due to its hepatotoxicity, immunotoxicity and carcinogenicity. However, the mechanism of its immunosuppressive effect is still under investigation. Dendritic cells (DCs) are the most potent professional antigen-presenting cells, and their differentiation, maturation and immunomodulatory functions are closely related to the immunotoxicity of certain mycotoxins. Migratory capacity is a prerequisite for mature DCs (mDCs) to move and present antigens in secondary lymphoid tissue, whereas the mechanical properties and cytoskeletal structure are critical for their migration and immune functions. Therefore, the effects of FB1 on the cell viability, mechanical characteristics, cytoskeletal structure and its binding proteins, migration, co-stimulatory molecules and the immune functions of mDCs were investigated to explore the potential mechanisms of immunotoxicity. The results showed that FB1 could impair the chemotactic migratory capability, the expression of co-stimulatory molecules and the ability of DCs to stimulate T cell proliferation. Further analyses elucidated that the mechanical properties of mDCs were changed, the cytoskeletal structures were reorganized and the expressions of cytoskeleton-binding proteins were regulated. In conclusion, the attenuated migration and immune functions of mDCs caused by FB1 may be related to their altered mechanical properties and cytoskeleton remodeling, which may be one of the action modes for FB1 to exert its immunosuppressive effect.