Format

Send to

Choose Destination
Clin Dev Immunol. 2012;2012:239368. doi: 10.1155/2012/239368. Epub 2012 Mar 6.

A key role for NF-κB transcription factor c-Rel in T-lymphocyte-differentiation and effector functions.

Author information

1
Institute for Medical Microbiology and Hygiene, Philipps University of Marburg, Hans Meerwein Strasse 2, 35032 Marburg, Germany. alexander.visekruna@staff.uni-marburg.de

Abstract

The transcription factors of the Rel/NF-κB family function as key regulators of innate and adoptive immunity. Tightly and temporally controlled activation of NF-κB-signalling pathways ensures prevention of harmful immune cell dysregulation, whereas a loss of control leads to pathological conditions such as severe inflammation, autoimmune disease, and inflammation-associated oncogenesis. Five family members have been identified in mammals: RelA (p65), c-Rel, RelB, and the precursor proteins NF-κB1 (p105) and NF-κB2 (p100), that are processed into p50 and p52, respectively. While RelA-containing dimers are present in most cell types, c-Rel complexes are predominately found in cells of hematopoietic origin. In T-cell lymphocytes, certain genes essential for immune function such as Il2 and Foxp3 are directly regulated by c-Rel. Additionally, c-Rel-dependent IL-12 and IL-23 transcription by macrophages and dendritic cells is crucial for T-cell differentiation and effector functions. Accordingly, c-Rel expression in T cells and antigen-presenting cells (APCs) controls a delicate balance between tolerance and immunity. This review gives a selective overview on recent progress in understanding of diverse roles of c-Rel in regulating adaptive immunity.

PMID:
22481964
PMCID:
PMC3310234
DOI:
10.1155/2012/239368
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Hindawi Limited Icon for PubMed Central
Loading ...
Support Center