Open AccessCurcumin modulation of IFN‐β and IL‐12 signalling and cytokine induction in human T cells
Author(s) -
Fahey Angela J.,
Adrian Robins R.,
Constantinescu Cris S.
Publication year - 2007
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2007.00089.x
Subject(s) - curcumin , stat4 , stat protein , cytokine , experimental autoimmune encephalomyelitis , phosphorylation , cancer research , chemistry , immunology , biology , stat , microbiology and biotechnology , immune system , pharmacology , stat3
Curcumin is a polyphenol derived from the dietary spice turmeric. It possesses diverse anti‐inflammatory and anti‐cancer properties. Curcumin has been shown to exhibit an inhibitory effect on the production of inflammatory cytokines by human monocytes and has inhibited the animal model of multiple sclerosis (MS), experimental autoimmune encephalomyelitis (EAE) in association with a decrease in interleukin 12 (IL‐12) production and signal transducer and activator of transcription 4 (STAT4) activation. The type I interferon (IFN) IFN‐has the ability to suppress IL‐12. Both IL‐12 and IFN‐α/β signal through the activation by phosphorylation of STAT4. Our aim was to investigate the effects of curcumin on the ability of T cells to respond to IL‐12 or IFN‐α/β. We report that curcumin decreases IL‐12‐induced STAT4 phosphorylation, IFN‐γ production, and IL‐12 Rβ1 and β2 expression. IFN‐β‐induced STAT4 phosphorylation, IL‐10 production and IFN receptor (IFNAR) subunits 1 and 2 expression were enhanced by curcumin. Curcumin increased IFN‐α‐induced IL‐10 and IFNAR1 expression. Prior exposure to curcumin decreased IFN‐α‐induced IFNAR2 expression and did not modify the level of IFN‐α‐induced pSTAT4 generation. Thus, the effect of curcumin on STAT4 activation in T cells is dependent upon the stimulus to which the T cells have been exposed.