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DC, when fully matured are the APC best able to activate naïve T cells. Recently, we demonstrated using adenoviruses overexpressing IkappaBalpha and proteosome inhibitors that NF-kappaB is involved in DC activation, but the role of the individual subunits is still not clear. We investigated the role of the NF-kappaB subunits RelB and p50 in human DC activation using adenoviral vectors expressing RelB or p50. Nuclear RelB, in the form of RelB/p50, was active only in DC infected with both viruses, this induced the production of the soluble homeostatic chemokine CCL19, but not other homeostatic chemokines, particularly in LPS-matured DC. However, RelB/p50 did not affect the expression of costimulatory and antigen-presenting molecules, and increased the allogeneic mixed lymphocyte reaction only in LPS-matured DC. This enhanced mixed lymphocyte reaction is most likely due to enhanced CCL19 production, which sustains the interaction between mature DC and naïve T cells. In conclusion, we demonstrated that RelB/p50 was active only in DC expressing both RelB and p50, and induced CCL19 production, but not DC maturation.

Original publication

DOI

10.1002/eji.200939209

Type

Journal article

Journal

European journal of immunology

Publication Date

08/2009

Volume

39

Pages

2215 - 2223

Addresses

Kennedy Institute of Rheumatology Division, School of Medicine, Imperial College London, London, UK.

Keywords

Antigen-Presenting Cells, Dendritic Cells, Humans, Adenoviridae, Lipopolysaccharides, Tumor Necrosis Factor-alpha, Green Fluorescent Proteins, Interleukin-6, Interleukin-10, Microscopy, Fluorescence, Blotting, Western, Enzyme-Linked Immunosorbent Assay, Transfection, Cell Differentiation, Binding Sites, Base Sequence, Protein Binding, I-kappa B Proteins, Transcription Factor RelB, NF-kappa B p50 Subunit, Chemokine CXCL13, Chemokine CCL19, Chemokine CCL22, NF-KappaB Inhibitor alpha