Key result
Enterovirus 71 infection activates the NLRP3 inflammasome in myeloid cells, while viral proteases 2A and 3C reciprocally cleave NLRP3 to counteract inflammasome activation.
Population
Mice in vivo and mammalian myeloid cells
Design
Preclinical
Authors
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Hypothesis-generating in mice; leaves open whether EV71 protease-mediated NLRP3 cleavage occurs in human infection.
Demonstrates a reciprocal regulatory mechanism where EV71 activates the NLRP3 inflammasome but simultaneously uses viral proteases to cleave NLRP3 and evade the immune response.
Wang et al. (2015) studied Enterovirus 71 (EV71) infection. Enterovirus 71 (EV71) infection was evaluated on NLRP3 inflammasome activation and IL-1β secretion. Enterovirus 71 infection activates the NLRP3 inflammasome in myeloid cells, while viral proteases 2A and 3C reciprocally cleave NLRP3 to counteract inflammasome activation.
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