title: Nuclear factor-κB in immunity and inflammation: the Treg and Th17 connection.
abstract: Although nuclear factor-kB (NF-kB) is generally considered to be a pro-inflammatory transcription factor, recent studies indicate that it also plays a critical role in the development of an anti-inflammatory T cell subset called regulatory T (Treg) cells. Two NF-kB proteins, c-Rel and p65, drive the development of Treg cells by promoting the formation of a Foxp3-specific enhanceosome. Consequently, c-Rel-deficient mice have marked reductions in Treg cells, and c-Rel-deficient T cells are compromised in Treg cell differentiation. However, with the exception of Foxp3, most NF-kB target genes in immune cells are pro-inflammatory. These include several Th17-related cytokine genes and the retinoid-related orphan receptor-g (Rorg or Rorc) that specifies Th17 differentiation and lineage-specific function. T cells deficient in c-Rel or p65 are significantly compromised in Th17 differentiation, and c-Rel -deficient mice are defective in Th17 responses. Thus, NF-kB is required for the development of both anti-inflammatory Treg and pro-inflammatory Th17 cells.
authors.affiliation: Department of Pathology and Laboratory Medicine, 712 Stellar-Chance Laboratories, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA. qingguo2@mail.med.upenn.edu
authors.forename: Qingguo
authors.initials: Q
authors.lastname: Ruan
authors.forename: Youhai H
authors.initials: YH
authors.lastname: Chen
mesh_terms: D000818:Animals; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D016328:NF-kappa B / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016328:NF-kappa B