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Kali
skiDepartment of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Glucocorticoids (GC) are known to affect the immune response at
several stages. However, little is known about how GC influence the
initiation of the specific immune response at the level of dendritic
cells (DC), the highly professional APC for T cells. Therefore, we
studied whether GC modulate the cytokine production and T cell
stimulatory function of DC. In LPS-stimulated DC, GC strongly reduced
the secretion of the Th1-skewing factor IL-12p70 and, to a lesser
extent, the production of the proinflammatory cytokines IL-6 and
TNF-
. Regarding the T cell stimulatory function of DC, GC did not
influence the cell surface expression of HLA-DR or the costimulatory
molecules CD40 and CD80 and did not influence the ability of DC to take
up Ag. Consequently, GC pretreatment of DC indeed did not affect their
ability to stimulate CD4+ Th cell proliferation in response
to superantigen. However, as a result of their defective production of
bioactive IL-12, GC-pretreated DC have a reduced ability to promote the
production of IFN-
in CD4+ Th lymphocytes, as shown by
the observation that IFN- production could be restored by exogenous
IL-12. In contrast, GC treatment of DC enhanced the secretion of the
antiinflammatory cytokine IL-10 and the type 2 cytokine IL-5 by the T
cells. It is concluded that, in addition to their role as potent
inhibitors of inflammation via the direct suppression of cytokine
production in T cells, GC may further inhibit T cell-mediated
inflammation indirectly via the suppression of IL-12 production by
DC.
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