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,
*
Department of Immunology and
Urological Institute, Cleveland Clinic Foundation, Cleveland, OH 44195;
Department of Biology, Case Western Reserve University, Cleveland, OH 44106; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106
During sensitization with dinitrofluorobenzene for contact
hypersensitivity (CHS) responses, hapten-specific CD8+ T
cells develop into IFN-
-producing cells, and CD4+ T
cells develop into IL-4/IL-5-producing cells. Administration of IL-12
during sensitization skews CD4+ T cell development to
IFN--producing cells, resulting in exaggerated CHS responses. In the
current report we tested the role of IL-12 on CD8+ T cell
development during sensitization and elicitation of CHS to
dinitrofluorobenzene. Administration of IL-12 during hapten
sensitization induced the expression of IL-12R
2 on both
CD4+ and CD8+ T cells, augmented IFN-
production by these T cell populations, and increased the magnitude and
duration of the CHS response to hapten challenge. CHS responses were
virtually identical in wild-type and IL-12 p40-/- mice.
Since engagement of CD40 on APC may stimulate IL-12 production, we also
tested the role of CD40-CD154 interactions on the development of
IFN--producing CD4+ and CD8+ T cells
following hapten sensitization. Development of IFN--producing
CD4+ T cells during hapten sensitization was absent in
wild-type mice treated with anti-CD154 mAb or in
CD154-/- mice. In contrast, the absence of CD40-CD154
signaling had little or no impact on the development of
IFN--producing CD8+ T cells. These results demonstrate
that the development of hapten-specific Th1 effector CD4+ T
cells in CHS requires both CD40-CD154 interactions and IL-12, whereas
the development of IFN--producing effector CD8+ T cells
can occur independently of these pathways.
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