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and IL-12 by STAT6-Dependent and -Independent Mechanisms1
The Biomedical Research Centre, University of British Columbia, Vancouver, BC, Canada
IL-4 promotes allergic responses and inhibits the production of
proinflammatory cytokines by monocytes and macrophages. The promotion
of allergic responses by IL-4 has been shown to be absolutely dependent
on the transcription factor STAT6. We report here that the inhibitory
effects of IL-4 on the production of TNF-
or IL-12 by macrophages
had both STAT6-dependent and -independent components, depending on the
stimuli. IL-4 failed to inhibit the release of TNF- or IL-12 from
STAT6 null macrophages stimulated with LPS alone. However, IL-4 still
induced significant inhibition of the production of TNF- and IL-12
from STAT6 null macrophages that were stimulated with the more
physiologically relevant combination of LPS and IFN-
. These data
show that STAT6 is required for the IL-4-mediated inhibition of the
production of TNF- and IL-12 stimulated by LPS alone, but that IL-4
also activates distinct, STAT6 independent mechanism(s) that inhibit
the IFN--mediated enhancement of IL-12 and TNF-
production.
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