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


ABSTRACT: 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.

SUBMITTER: Parra M 

PROVIDER: S-EPMC7473529 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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

Parra Marcela M   Weitner Megan M   Yang Amy A   Akue Adovi A   Liu Xia X   Schmidt Thomas T   Allman Windy R WR   Akkoyunlu Mustafa M   Derrick Steven C SC  

PloS one 20200904 9


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  ...[more]

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