PD-L2 negatively regulates Th1-mediated immunopathology during Fasciola hepaticainfection

STEMPIN, C; MOTRAN, C; AOKI, MP; FALCON, C; CERBAN, FM; CERVI, L

Oncotarget

Oncotarget editorial

Año: 2016

1949-2553

acrophage plasticity is critical for controlling inflammation including those produced by helminth infections, where alternatively activated macrophages (AAM) are accumulated in tissues. AAM expressing the co-inhibitory molecule programmed death ligand 2 (PD-L2), which is capable of binding programmed death 1 (PD-1) expressed on activated T cells, have been demonstrated in different parasitic infections. However, the role of PD-L2 during F. hepaticainfection has not yet been explored. We observed that F. hepaticainfection or a F. hepaticatotal extract (TE) injection increased the expression of PD-L2 on peritoneal macrophages. In addition, the absence of PD-L2 expression correlated with an increase in susceptibility to F. hepaticainfection, as evidenced by the shorter survival and increased liver damage observed in PD-L2 deficient (KO) mice. We assessed the contribution of the PD-L2 pathway to Th2 polarization during this infe