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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 respon...

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Bibliographic Details
Published in:PloS one 2020-09, Vol.15 (9), p.e0238493-e0238493
Main Authors: Parra, Marcela, Weitner, Megan, Yang, Amy, Akue, Adovi, Liu, Xia, Schmidt, Thomas, Allman, Windy R., Akkoyunlu, Mustafa, Derrick, Steven C.
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Language:English
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0238493