Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB
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...
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| Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 106; no. 35; pp. 14978 - 14983 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
National Academy of Sciences
01.09.2009
National Acad Sciences |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0027-8424 1091-6490 1091-6490 |
| DOI | 10.1073/pnas.0809784106 |
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| 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. |
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| AbstractList | 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. |
| Author | Porta, Chiara De Baetselier, Patrick Sica, Antonio Ghezzi, Pietro Ghisletti, Serena Mantovani, Alberto Raes, Geert Rimoldi, Monica Dieli, Francesco Di Liberto, Diana Natoli, Gioacchino Brys, Lea |
| Author_xml | – sequence: 1 fullname: Porta, Chiara – sequence: 2 fullname: Rimoldi, Monica – sequence: 3 fullname: Raes, Geert – sequence: 4 fullname: Brys, Lea – sequence: 5 fullname: Ghezzi, Pietro – sequence: 6 fullname: Di Liberto, Diana – sequence: 7 fullname: Dieli, Francesco – sequence: 8 fullname: Ghisletti, Serena – sequence: 9 fullname: Natoli, Gioacchino – sequence: 10 fullname: De Baetselier, Patrick – sequence: 11 fullname: Mantovani, Alberto – sequence: 12 fullname: Sica, Antonio |
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