期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2009
卷号：106
期号：35
页码：14978-14983
DOI：10.1073/pnas.0809784106
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：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-{kappa}B 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-{kappa}B as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-{kappa}B inhibits NF-{kappa}B-driven, M1-polarizing, IFN-{beta} 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-{kappa}B p50 is a key component in the orchestration of M2-driven inflammatory reactions.
