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Department of Pediatrics, Stanford University, Stanford, CA 94305
We investigated the effects of corticosteroids on IL-12 production
by mouse splenic adherent cells and the subsequent capacity of these
cells to induce cytokine production by CD4+ T cells.
To distinguish the effects of corticosteroids on APCs from those on T
cells, only the APCs and not the T cells were exposed to
corticosteroids. Treatment of splenic adherent cells with dexamethasone
greatly inhibited production of IL-12, a cytokine known to enhance
IFN-
synthesis and decrease IL-4 synthesis by CD4+ T
cells. The reduction in IL-12 production by corticosteroid-treated
macrophages decreased their ability to induce IFN- and increased
their ability to induce IL-4 synthesis in Ag-primed CD4+ T
cells. Splenic adherent cells from mice treated in vivo with
dexamethasone also displayed a reduced capacity to produce IL-12. These
results help to resolve previous conflicting observations regarding the
effects of corticosteroids on cytokine production by T cells, and
indicate that while corticosteroids may directly inhibit Th1 and Th2
cytokine production in T cells, corticosteroids, by reducing IL-12
production in APCs, have the potential to indirectly enhance Th2
cytokine synthesis. Therefore, treatment of diseases such as allergy
with chronic corticosteroids may indirectly exacerbate the course of
the disease, which is caused primarily by the overproduction of Th2
cytokines in allergen-specific CD4+ T cells.
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