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The Journal of Immunology, Vol 155, Issue 2 836-844, Copyright © 1995 by American Association of Immunologists
ARTICLES |
JJ Lorenz, PJ Furdon, JD Taylor, MW Verghese, G Chandra, TA Kost, SA Haneline, LA Roner and JG Gray
Department of Cell Physiology, Glaxo Wellcome, Inc., Research Triangle Park, NC 27709, USA.
IL-1 beta is a cytokine generally considered to be a major component involved in the pathogenesis of rheumatoid arthritis and other inflammatory diseases. Of the agents found in high concentrations in inflamed rheumatoid arthritis joints, TNF-alpha is among the most strongly implicated as an in vivo inducer of IL-1 beta. Here we report that in human PBMC and in a stable transfectant of the promonocytic cell line, THP-1, TNF-alpha indeed appears to be an inducer of IL-1 beta production, but only in the presence of dibutyryl cAMP or agents such as the PG that elevate intracellular cAMP levels. This TNF- alpha/cAMP pathway regulates IL-1 beta production at the level of transcription and requires a cAMP response element located between - 2762 and -2755 bp in the upstream regulatory sequence of IL-1 beta. Because PG, which are known to elevate cAMP levels in vivo, and TNF- alpha are both found in significant quantities in the synovial fluid of rheumatoid arthritis joints, the observed synergistic up-regulation in IL-1 beta synthesis by TNF-alpha/cAMP (PG) may provide valuable insight into the potential pathways involved in the continuous production of IL- 1 beta in the chronically inflamed joint.
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