Memory CD73(+)IgM(+) B cells protect against Plasmodium yoelii infection and express Granzyme B

To better understand anti-malaria protective immune responses, we examined the cellular mechanisms that govern protective immunity in a murine Plasmodium yoelii 17X NL (PyNL) re-infection model. Initially, we confirmed that immune B cells generated during a primary PyNL infection were largely responsible for protection from a second PyNL infection. Using the previously identified memory B cell markers CD80, PD-L2, and CD73, we found an increase in the frequency of CD80(-)PD-L2(-)CD73(+) B cells up to 55 days after a primary PyNL infection and at 4–6 days following a second PyNL infection. Moreover, injection of enriched immune CD19(+)CD73(+) B cells into nonimmune mice were significantly more protective against a PyNL infection than CD73(-) B cells. Interestingly, a substantial fraction of these CD73(+) B cells also expressed IgM and granzyme B, a biomolecule that has been increasingly associated with protective responses against malaria.