Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

Chiara Porta, Monica Rimoldi, Geert Raes, Lea Brys, Pietro Ghezzi, Diana Di Liberto, Francesco Dieli, Serena Ghisletti, Gioacchino Natoli, Patrick De Baetselier, Alberto Mantovani, Antonio Sica

Research output: Contribution to journalArticlepeer-review

Abstract

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-κB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-κB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-κB inhibits NF-κB-driven, M1-polarizing, IFN-β production. Accordingly, p50-deficient mice show exacerbated M1-driven inflammation and defective capacity to mount allergy and helminth-driven M2-polarized inflammatory reactions. Thus, NF-κB p50 is a key component in the orchestration of M2-driven inflammatory reactions.

Original languageEnglish
Pages (from-to)14978-14983
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume106
Issue number35
DOIs
Publication statusPublished - Sep 1 2009

ASJC Scopus subject areas

  • General

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