PD-L2 regulates arginase induction and modifies Trypanosoma cruzi survival in macrophages during murine experimental infection.

DULGERIAN L.1; GARRIDO V.2; STEMPIN C.3; CERBÁN F.4

WILEY-BLACKWELL PUBLISHING, INC

Año: 2011 vol. 133 p. 29 - 29

he programmed death ligand 1 (PD-L1) and 2 (PD-L2) that bind to the receptor programmed death 1 (PD-1) have been involved in peripheral tolerance and in the immune escape mechanisms during chronic viral infections and cancer. However, there are no reports about the role of these molecules during Trypanosoma cruzi infection. We have studied the role of PD-L1 and PD-L2 in T. cruzi infection and its importance in arginase/inducible nitric oxide synthase (iNOS) balance in the immunomodulatory properties of macrophages (Mo). In this work, we have demonstrated that PD-1/PD-Ls pathway expression is modified during T. cruzi infection on Mos obtained from the peritoneal cavity. Mos from T. cruzi-infected mice suppressed T cells proliferation and it was restored when anti-PD-1 and anti-PD-L1 antibodies were added. Nevertheless, anti-PD-L2 antibody treatment did not re-establish T cell proliferation. PD-L2 blockade on peritoneal cells from infected mice showed an increase in arginase expression