The fact that i) the kinetics of infection was comparable in Py-infected PD-1-/-, PD-L1-/-, heterozygous and WT littermate mice, and ii) we did not find any differences in either T, B cell or Ab responses despite extensive analyses, suggests that genetic deficiency in PD-1 and PD-L1 may favor the utilization of distinct mechanisms of resistance against this infection through otherwise redundant pathways. Here, CD274 is linked to infection.