Inflammation, when properly mounted and precisely calibrated, is a beneficial process that enables the rapid removal of invading pathogens and/or cellular corpses and promotes tissue repair/regeneration to restore homeostasis after injury. Being a paradigm of a rapid response transcription factor, the nuclear factor-kappa B (NF-κB) transcription factor family plays a central role in amplifying inflammation by inducing the expression of inflammatory cytokines and chemokines. Additionally, NF-κB also induces the expression of pro-survival and -proliferative genes responsible for promoting tissue repair and regeneration. Paradoxically, recent studies have suggested that the NF-κB pathway can also exert inhibitory effects on pro-inflammatory cytokine production to temper inflammation. Here, we review our current understanding about the pro- and anti-inflammatory roles of NF-κB and discuss the implication of its dichotomous inflammation-modulating activity in the context of inflammasome activation and tumorigenesis.
Zhenyu Zhong, Atsushi Umemura, Elsa Sánchez‐López, Shuang Liang, Shabnam Shalapour, Jerry Wong, Feng He, Daniela Boassa, Guy Perkins, Syed R. Ali, Matthew G McGeough, Mark H. Ellisman, Ekihiro Seki, Åsa B. Gustafsson, Hal M. Hoffman, María T. Díaz‐Meco, Jorge Moscat, Michael Karin
Mónica Gumà, Dariusz Stepniak, Helena Shaked, Martina E. Spehlmann, Steve Shenouda, Hilde Cheroutre, Ildelfonso Vicente-Suarez, Lars Eckmann, Martin F. Kagnoff, Michael Karin
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