More to Life than NF-κB in TNFR1 Signaling

Adrian T. Ting, Mathieu J.M. Bertrand

Research output: Contribution to journalReview articlepeer-review

94 Scopus citations

Abstract

TNF is a master proinflammatory cytokine whose pathogenic role in inflammatory disorders has long been attributed to induction of proinflammatory mediators. TNF also activates cell survival and death pathways, and recent studies demonstrated that TNF also causes inflammation by inducing cell death. The default response of most cells to TNF is survival and NF-κB-mediated upregulation of prosurvival molecules is a well-documented protective mechanism downstream of TNFR1. Recent studies revealed the existence of an NF-κB-independent cell death checkpoint that restricts cell demise by inactivating RIPK1. Disruption of this checkpoint leads to RIPK1 kinase-dependent death and causes inflammation in vivo. These revelations bring complexity to the control of TNF-induced cell death, and suggest clinical benefit of RIPK1 inhibitors in TNF-driven human inflammatory disorders.

Original languageEnglish (US)
Pages (from-to)535-545
Number of pages11
JournalTrends in Immunology
Volume37
Issue number8
DOIs
StatePublished - Aug 1 2016

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Fingerprint Dive into the research topics of 'More to Life than NF-κB in TNFR1 Signaling'. Together they form a unique fingerprint.

Cite this