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*
Interdisciplinary Program in Immunology and
Department of Microbiology, University of Iowa, Iowa City, IA 52242
In vivo priming of CD8+ T lymphocytes against
exogenously processed model Ags requires CD4+ T cell help,
specifically interactions between CD40 ligand (CD40L) expressed by
activated CD4+ T cells and CD40, which is present on
professional APC such as dendritic cells (DCs). To address this issue
in the context of bacterial infection, we examined CD40L-CD40
interactions in CD8+ T cell priming against an exogenously
processed, nonsecreted bacterial Ag. CD40L interactions were blocked by
in vivo treatment with anti-CD40L mAb MR-1, which inhibited
germinal center formation and CD8+ T cell cross-priming
against an exogenous model Ag, OVA. In contrast, MR-1 treatment did not
interfere with CD8+ T cell priming against a nonsecreted or
secreted recombinant Ag expressed by Listeria
monocytogenes. Memory and secondary responses of
CD8+ T cells against nonsecreted and secreted bacterial Ags
were also largely unimpaired by transient MR-1 treatment. When
MR-1-treated mice were concurrently immunized with L.
monocytogenes and OVA-loaded splenocytes, cross-priming of
OVA-specific naive CD8+ T cells occurred. No significant
decline in cross-priming against OVA was measured when either TNF or
IFN-
was neutralized in L. monocytogenes-infected
animals, demonstrating that multiple signals exist to overcome CD40L
blockade of CD8+ T cell cross-priming during bacterial
infection. These data support a model in which DCs can be stimulated in
vivo through signals other than CD40, becoming APC that can effectively
stimulate CD8+ T cell responses against exogenous Ags
during infection.
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