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*
Department of Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106
The primary effector cells of contact hypersensitivity (CHS)
responses to dintrofluorobenzene (DNFB) are IFN-
-producing
CD8+ T cells, whereas CD4+ T cells regulate the
magnitude and duration of the response. The requirement for CD40-CD154
engagement during CD8+ and CD4+ T cell priming
by hapten-presenting Langerhans cells (hpLC) is undefined and was
tested in the current study. Similar CHS responses to DNFB were
elicited in wild-type and CD154-/- animals. DNFB
sensitization of CD154-/- mice primed IFN--producing
CD8+ T cells and IL-4-producing CD4+ T cells.
However, anti-CD154 mAb MR1 given during hapten sensitization
inhibited hapten-specific CD8+, but not CD4+, T
cell development and the CHS response to challenge. F(ab')2
of MR1 failed to inhibit CD8+ T cell development and the
CHS response suggesting that the mechanism of inhibition is distinct
from that of CD40-CD154 blockade. Furthermore, anti-CD154 mAb did
not inhibit CD8+ T cell development and CHS responses in
mice depleted of CD4+ T cells or in CD4-/-
mice. During in vitro proliferation assays, hpLC from mice treated with
anti-CD154 mAb during DNFB sensitization were less stimulatory for
hapten-primed T cells than hpLC from either control mice or mice
depleted of CD4+ T cells before anti-CD154 mAb
administration. These results demonstrate that development of
IFN--producing CD8+ T cells and the CHS response are not
dependent on CD40-CD154 interactions. This study proposes a novel
mechanism of anti-CD154 mAb-mediated inhibition of CD8+
T cell development where anti-CD154 mAb acts indirectly through
CD4+ T cells to impair the ability of hpLC to prime
CD8+ T cells.
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