PD-1 deficiency impairs eosinophil recruitment and cytotoxicity to muscle larvae of Trichinella spiralis

Description

Blockade of PD-1 may serve as a promising strategy in controlling pathogen infections through enhancing host immune cell function. Eosinophils are the essential components of the type 2 immune mechanism that function in host defense against helminth infections. Here we examine the role of PD-1 in eosinophilia in mice during T. spiralis infection. Unexpectedly, PD-1 deficient (PD-1-/-) mice developed higher muscle larvae loads and exacerbated disease compared to wild type mice. Further study showed that PD-1 deficiency impaired the recruitment of eosinophils into the parasite invaded tissue and their cytotoxicity to muscle larvae through reduced production of eosinophil-specific chemokines, and expression of adhesion molecules intergrin α4β7 and L-selectin on eosinophils and VCAM-1 on vascular endothelial cells after T. spiralis infection. The compromised T-helper 2 (Th2) cytokine response contributed to the impaired adhesion interactions involved in eosinophil migration in PD-1-/- mice infected with T. spiralis. Our data revealed the positive role of PD-1 in host defense against helminth infection by regulating the migration and trafficking of eosinophils to the infection site.

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