A role for chondroitin sulphate B in the activity of interleukin 12 in stimulating gamma-interferon secretion.
We show, using a murine NK cell line which responds quantitatively to rmIL-12, that treatment with ChABCase, but not other GAGases, results in substantial reductions in the secretion of gamma-IFN. Likewise, treatment of the cells with a beta-D-xyloside inhibitor of proteoglycan biosynthesis inhibits this cytokine response. In both treatments, the addition of soluble, exogenous GAGs does not relieve the inhibition of gamma-IFN secretion. We also demonstrate by ELISA that rmIL-12 binds to CS B. Overall, our studies on this in vitro cellular model of the initiation of Th1 immune responses indicate a major role for cell-surface, iduronate-rich, CS proteoglycan in the biological activity of IL-12.
Garnier
Pascale
P
School of Biological Sciences, Royal Holloway University of London, Egham Hill, Surrey TW200EX, Egham, UK.
Gibbs
Roslyn V
RV
Rider
Christopher C
CC
D000818:Animals; D002454:Cell Differentiation / Q000187:drug effects; D003871:Dermatan Sulfate / Q000502:physiology*; D004797:Enzyme-Linked Immunosorbent Assay; D066298:In Vitro Techniques; D007371:Interferon-gamma / Q000378:metabolism*; D018664:Interleukin-12 / Q000494:pharmacology*; D007694:Killer Cells, Natural / Q000187:drug effects* / Q000378:metabolism; D051379:Mice
D018664:Interleukin-12; D003871:Dermatan Sulfate; D007371:Interferon-gamma