A novel “complement–metabolism–inflammasome axis” as a key regulator of immune cell effector function

Giuseppina Arbore, Claudia Kemper*

*Corresponding author for this work
123 Citations (Scopus)

Abstract

The inflammasomes are intracellular multiprotein complexes that induce and regulate the generation of the key pro-inflammatory cytokines IL-1β and IL-18 in response to infectious microbes and cellular stress. The activation of inflammasomes involves several upstream signals including classic pattern or danger recognition systems such as the TLRs. Recently, however, the activation of complement receptors, such as the anaphylatoxin C3a and C5a receptors and the complement regulator CD46, in conjunction with the sensing of cell metabolic changes, for instance increased amino acid influx and glycolysis (via mTORC1), have emerged as additional critical activators of the inflammasome. This review summarizes recent advances in our knowledge about complement-mediated inflammasome activation, with a specific focus on a novel “complement – metabolism – NLRP3 inflammasome axis.”.

Original languageEnglish
JournalEuropean Journal of Immunology
Volume46
Issue number7
Pages (from-to)1563-1573
Number of pages11
ISSN0014-2980
DOIs
Publication statusPublished - 01.07.2016

Funding

Work in the Kemper laboratory is supported by the MRC Centre. Grant MR/J006742/1, an EU-funded Innovative Medicines Initiative BTCURE (C.K.), a Wellcome Trust Investigator Award (C.K.), and the King's Bioscience Institute at King's College London (G.A.), the National Institute for Health Research (NIHR) Biomedical Research Centre based at Guy's and St. Thomas' NHS Foundation Trust and King's College London, and by the Division of Intramural Research, National Heart, Lung, and Blood Institute, NIH and the intramural research program of NIAID, NIH.

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)

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