Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.1006633 on March 9, 2007

Published online before print March 9, 2007
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(Journal of Leukocyte Biology. 2007;81:1562-1567.)
© 2007 by Society for Leukocyte Biology

Reciprocal effects of IFN-ß and IL-12 on STAT4 activation and cytokine induction in T cells

Angela J. Fahey*, R. Adrian Robins{dagger} and Cris S. Constantinescu*,1

Divisions of
* Clinical Neurology and
{dagger} Molecular and Clinical Immunology, University of Nottingham, Nottingham, United Kingdom

1 Correspondence: Division of Clinical Neurology, Queens Medical Centre, Medical School, University of Nottingham, Nottingham NG7 2UH, UK. E-mail: cris.constantinescu{at}nottingham.ac.uk

IL-12 is an immunoregulatory cytokine, which promotes Th1 cell differentiation and is a major inducer of IFN-{gamma}. IFN-ß, a Type I IFN used in the treatment of multiple sclerosis, has been shown to significantly increase the expression of the anti-inflammatory cytokine IL-10, a major suppressor of Th1 cytokines. The beneficial immunomodulatory effects of IFN-ß may in part be a result of its ability to suppress IL-12. However, IL-12 and IFN-ß signal via the STAT4 pathway. Our aim was to investigate the relationship between IL-12 and IFN-ß by observing the effect of prior exposure to IL-12 or IFN-ß on the ability of T cells to subsequently respond to the other cytokine. We report that IFN-ß increases IL-12-induced STAT4 phosphorylation and up-regulates IL-12 receptor ß1 and ß2 expression. However, despite this up-regulation, IFN-ß suppressed IL-12-induced IFN-{gamma} expression. Our results suggest that this may be a result of the parallel induction of IL-10 by IFN-ß.

Key Words: human • signal transduction • IFN-gamma • interleukin-10






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