Programmed cell death-1 ligand 2: the other PD-1 ligand

6 Apr 2017
Monash University, Level 3 Seminar Room 15 Innovation Walk, Clayton campus

About this seminar

Many pathogens, including Plasmodium spp., which cause malaria, exploit the programmed death-1 (PD-1)/ PD-L1 pathway to 'deactivate' T cell functions but the role of PD-1/PD-L2 remains unclear. We studied malarial infections to understand the contribution of PD-L2 to immunity. Here we show that higher PD- L2 expression on blood dendritic cells, from Plasmodium falciparum-infected individuals, correlated with lower parasitemia. Mechanistic studies in mice showed that PD-L2 was indispensable for establishing effective CD4+ Th1 immunity. Importantly, administration of soluble PD-L2 to mice with lethal malaria was sufficient to dramatically improve immunity and survival (92% vs 0%). These studies show a new function for PD- L2, which has potential to be translated into an effective treatment for malaria and other diseases where T cell immunity is ineffective or short-lived due to PD-1. 

About the presenter

Michelle Wykes is head of the Molecular Immunology Laboratory at the QIMR Berghofer Medical Research Institute in Brisbane. She studies the mechanisms by which Plasmodium spp, which cause malaria, are able to evade immunity. Her recent research has focused on the Programmed cell death pathway (PD-1) and how PD-L2 is crucial for establishing effective CD4+ Th1 immunity against malaria. This line of research, published recently in Immunity, has potential to be used as a novel therapeutic for this infectious disease. 

More information

Time: 12 - 1pm

Host: Colby Zaph

Presented by: Monash Biomedicine Discovery Institute