TAK1ng control: TAK1 restrains NLRP3 activation

Matthew Stephen Mangan; Eicke Latz

doi:10.1084/jem.20180282

TAK1ng control: TAK1 restrains NLRP3 activation

J Exp Med. 2018 Apr 2;215(4):1007-1008. doi: 10.1084/jem.20180282. Epub 2018 Mar 5.

Authors

Matthew Stephen Mangan^{1

2}, Eicke Latz^{3

4

2}

Affiliations

¹ Institute of Innate Immunity, University of Bonn, Bonn, Germany.
² German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
³ Institute of Innate Immunity, University of Bonn, Bonn, Germany eicke.latz@uni-bonn.de.
⁴ Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA.

Abstract

In this issue of JEM, Malireddi et al. (https://doi.org/10.1084/jem.20171922) demonstrate that macrophage-specific loss of TAK1 causes spontaneous NLRP3 inflammasome activation, driven by unregulated TNF secretion and signaling. This has implications for therapeutically targeting TAK1, enhancing its potential function as an anticancer drug treatment.

Publication types

Comment

MeSH terms

Cell Death
Cell Proliferation
Inflammasomes*
Macrophages*
NLR Family, Pyrin Domain-Containing 3 Protein

Substances

Inflammasomes
NLR Family, Pyrin Domain-Containing 3 Protein