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[摘要]：Methods. In order to ascertain the stimulatory capacity of primary human monocyte-derived DCs infected with wild-type DENV isolates, representing a range of genotypes and disease outcomes, we cocultured infected DCs with allogeneic-naive CD4(+) T cells. The gene expression patterns of IFN-alpha/beta sensitive genes were quantitated to determine if the infected DCs displayed a blunted IFN-alpha/beta response. Results. DENV-infected DCs induced the initial proliferation of naive CD4(+) T cells but they remained nonpolarized in effector function. The expression of IFN-alpha/beta-stimulated genes was downregulated, revealing that the inhibition of IFN-alpha/beta signaling is conserved among endemic DENV serotype 2 strains. Conclusions. The failure of naive CD4(+) T cells to differentiate into IFN gamma-producing effector T cells when primed by DENV-infected DCs cannot be explained solely by a block in IFN-alpha/beta signaling, suggesting that the ability of DENV to evade the early host response is multifaceted. |
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