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.