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Updated: Dec 26, 2025
Isolation And Dendritic Cell-Uptake of Small Extracellular Vesicles from Echinococcus granulosus
Published on: March 28, 2025
Echinococcus multilocularis vesicular fluid induces the expression of immune checkpoint proteins in vitro
Anne-Pauline Bellanger1,2,3, Sandra Courquet1,2,3, Jean-René Pallandre4
1Parasitology Mycology Department, Jean Minjoz University Hospital, Besancon, France.
Insights
Echinococcus multilocularis vesicular fluid increases immune checkpoint expression on NK and T cells. This suggests a mechanism for parasite immune evasion in alveolar echinococcosis.
Area of Science:
- Immunology
- Parasitology
- Infectious Diseases
Background:
- Alveolar echinococcosis is a severe chronic parasitic infection.
- The infection presents with tumor-like pathology.
- Understanding host-parasite immune interactions is crucial.
Purpose of the Study:
- To investigate in vitro interactions between Echinococcus multilocularis vesicular fluid (VF) and immune checkpoints.
- To analyze the expression of PD-1/PD-L1, CTLA-4, LAG-3, and TIM-3.
- To explore potential immune evasion strategies of E. multilocularis.
Main Methods:
- Peripheral blood mononuclear cells (PBMC) from healthy donors were isolated.
- Natural killer (NK) cells and T cells were stimulated with E. multilocularis-VF.
- Immune checkpoint expression was measured by flow cytometry.
- Cytokine levels in supernatants were analyzed using immunoassays.
Main Results:
- E. multilocularis-VF significantly increased PD-1, PD-L1, LAG-3, and TIM-3 expression on NK cells.
- PD-L1 and CTLA-4 expression increased on T cells following VF exposure.
- Increased Th1 and Th2 cytokine levels were observed in T cell supernatants.
Conclusions:
- Preliminary data suggest immune checkpoints are modulated by E. multilocularis.
- This modulation may represent a mechanism for immune evasion during alveolar echinococcosis.
- Further research is warranted to elucidate the role of immune checkpoints in this disease.
Aims:
Alveolar echinococcosis is a severe chronic helminthic infection that mimics a tumour-like disease. This study aimed at investigating in vitro interactions between Echinococcus multilocularis vesicular fluid (VF) and different immune checkpoints (PD-1/PD-L1, CTLA-4, LAG-3 and TIM-3).
Methods And Results:
Peripheral blood mononuclear cells (PBMC) from healthy blood donors were isolated by Ficoll. Natural killer (NK) cells were selected. Each type of cell was stimulated individually with E. multilocularis-VF. Expression of the different immune checkpoints was measured by flow cytometry on day 3 and day 6; all supernatants were used for immunoassays. Cells and supernatants from 22 healthy donors were analysed. A significant increase of PD-1, PD-L1, LAG-3 and TIM-3 was observed upon E. multilocularis-VF exposure for NK cells on day 3 (P < .05, Wilcoxon signed-rank test). A significant increase of PD-L1 and CTLA-4 was observed upon E. multilocularis-VF exposure for T cells on day 6 (P < .05, Wilcoxon signed-rank test), which was associated with increased levels of Th1 and Th2 cytokines P < .05, Wilcoxon signed-rank test).
Conclusion:
These preliminary data suggest that immune checkpoints could be a way for E. multilocularis to modulate the host immune response during alveolar echinococcosis.
