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The signaling adaptor BCAP inhibits NLRP3 and NLRC4 inflammasome activation in macrophages through interactions with

Samuel J Carpentier1, Minjian Ni2, Jeffrey M Duggan2,3

  • 1Department of Microbiology, University of Washington, Seattle, WA 98195, USA.

Science Signaling
|May 16, 2019
PubMed

Insights

B cell adaptor for phosphoinositide 3-kinase (BCAP) inhibits inflammasome activation in macrophages. This adaptor protein plays a key role in pathogen sensing and immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • B cell adaptor for phosphoinositide 3-kinase (BCAP) is a signaling adaptor protein.
  • BCAP activates the PI3K pathway downstream of B cell receptor and Toll-like receptor signaling.
  • BCAP interacts with the p85 regulatory subunit of class I PI3K.

Purpose of the Study:

  • To identify BCAP-interacting proteins in macrophages.
  • To investigate the role of BCAP in inflammasome function.
  • To elucidate the mechanism by which BCAP regulates inflammasome activation.

Main Methods:

  • Proteomic analysis to identify BCAP-interacting proteins.
  • Investigated BCAP's role in NLRP3- and NLRC4-induced inflammasome activation.
  • Assessed caspase-1 activation, cell death, and IL-1β release in macrophages.
  • Utilized BCAP-deficient mice to study Yersinia pseudotuberculosis clearance.

Main Results:

  • BCAP specifically associated with Flightless-1 and leucine-rich repeat flightless-interacting protein 2.
  • BCAP inhibited NLRP3- and NLRC4-induced caspase-1 activation, cell death, and IL-1β release.
  • BCAP-deficient mice showed enhanced clearance of Yersinia pseudotuberculosis.
  • BCAP delayed pro-caspase-1 recruitment and activation within the inflammasome.

Conclusions:

  • BCAP is a multifunctional signaling adaptor that inhibits key pathogen-sensing pathways in macrophages.
  • BCAP's inhibition of inflammasome activation is mediated through its association with Flightless-1.
  • BCAP plays a critical role in regulating innate immune responses to bacterial pathogens.

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