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1
Division of Infectious Diseases, University of Cincinnati College of Medicine, Cincinnati, OH 45267
We studied how the interaction between human dendritic cells (DC)
and Toxoplasma gondii influences the generation of
cell-mediated immunity against the parasite. We demonstrate that
viable, but not killed, tachyzoites of T. gondii altered
the phenotype of immature DC. DC infected with viable parasites
up-regulated the expression of CD40, CD80, CD86, and HLA-DR and
down-regulated expression of CD115. These changes are indicative of DC
activation induced by T. gondii. Viable and killed
tachyzoites had contrasting effects on cytokine production. DC infected
with viable T. gondii rather than DC that phagocytosed
killed parasites induced secretion of high amounts of IFN-
by T
cells from T. gondii-seronegative donors. IFN-
production in response to DC infected with viable parasites required
CD28 and CD40 ligand (CD40L) signaling. In addition, this IFN-
response was dependent in part on IL-12 secretion. Production of IL-12
p70 occurred after interaction between T cells and DC infected with
viable T. gondii, but not after incubation of T cells
with DC plus killed tachyzoites. IL-12 synthesis was inhibited by
blockade of CD40L signaling. IL-12-independent IFN- production
required CD80/CD86-CD28 interaction and, to a lesser extent, CD40-CD40L
signaling. Taken together, T. gondii-induced activation
of human DC is associated with T cell production of IFN- through
CD40-CD40L-dependent release of IL-12 and through CD80/CD86-CD28 and
CD40-CD40L signaling that mediate IFN- secretion even in the absence
of bioactive IL-12.
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