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Adv Exp Med Biol. 2012;946:207-21. doi: 10.1007/978-1-4614-0106-3_12.

Nuclear factor-κB in immunity and inflammation: the Treg and Th17 connection.

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1
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

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.

PMID:
21948370
DOI:
10.1007/978-1-4614-0106-3_12
[Indexed for MEDLINE]
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