Blockade

Metacestode

Immune system

Biochemistry

Receptor

Immunotherapy

Echinococcus multilocularis

Biology

Zoology

Helminths

Echinococcosis

Cestoda

Immunology

Parasite Immunology

Summary The growth potential of the tumour‐like Echinococcus multilocularis metacestode (causing alveolar echinococcosis, AE ) is directly dependent upon the nature/function of the periparasitic adaptive host immune‐mediated processes. PD ‐1/ PD ‐L1 pathway (programmed cell death 1), which inhibits lymphocytic proliferation in tumour development, is over‐expressed at the chronic stage of AE . We tested the impact of a PD ‐1/ PD ‐L1 pathway blockade on the outcome of both chronic AE (intraperitoneal metacestode inoculation, secondary AE and SAE ) and acute AE (peroral egg infection, primary AE and PAE ). To assess the parasite proliferation potential, we measured parasite mass weight for SAE and liver lesion number for PAE . In both models, the parasite load was significantly decreased in response to anti‐ PD ‐L1 antibody treatment. In SAE , anti‐ PDL 1 administration was associated with increased Th1 response parameters and decreased Treg responses, while in PAE anti‐ PDL 1 administration was associated with fewer lesions in the liver and decreased Treg/Th2 responses. Our findings highly suggested that a PD ‐1/ PD ‐L1 pathway blockade triggered the host immune responses in favour of an immune‐mediated control of E. multilocularis proliferation. Based on this, future studies that combine PD ‐1/ PD ‐L1 blockade with a parasitostatic albendazole medication may yield in a putatively curative therapeutic approach to control alveolar echinococcosis.

Immunotherapy of alveolar echinococcosis via <scp>PD</scp>‐1/<scp>PD</scp>‐L1 immune checkpoint blockade in mice

Immunotherapy of alveolar echinococcosis via PD‐1/PD‐L1 immune checkpoint blockade in mice