The Brucella effector protein TcpB induces degradation of inflammatory caspases and thereby subverts non-canonical inflammasome activation in macrophages.

ABSTRACT: The inflammasome contains intracellular receptors that recognize various pathogen-associated molecular patterns and play crucial roles in innate immune responses to invading pathogens. Non-canonical inflammasome activation is mediated by caspase-4/11, which recognizes intracellular LPS and promotes pyroptosis and secretion of proinflammatory cytokines. Brucella species are infectious intracellular pathogens that replicate in professional and non-professional phagocytic cells and subvert immune responses for chronic persistence in the host. The Brucella effector protein TcpB suppresses Toll-like receptor 2 (TLR2)- and TLR4-mediated innate immune responses by targeted degradation of the Toll/interleukin-1 receptor (TIR) domain-containing adaptor protein. TcpB is a cell-permeabl

SUBMITTER: Jakka P 

PROVIDER: S-EPMC5733597 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature