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*
Department of Molecular Genetics, Chiba University Graduate School of Medicine; and
First Department of Internal Medicine, Chiba University School of Medicine, Chiba, Japan
It has recently been established that FcRs are involved in the
triggering of type II and III inflammatory responses. Although FcR is
not believed to be involved in the regulation of T cell function, the
in vivo contribution of FcRs to T cell function still remains unclear.
We analyzed in vivo responses of delayed-type hypersensitivity and
proliferation of CD4+ T cells to Ags in
FcR
-/- mice lacking the expression and
function of FcRI, FcRIII, and Fc
RI. We found that the
delayed-type hypersensitivity response in
FcR-/- mice is significantly decreased
compared with that in wild-type mice. Moreover, the secondary responses
of proliferation and cytokine production as well as the Ab formation by
CD4+ T cells from FcR-/- mice
to Ag and normal APCs were also reduced. In contrast, in vitro primary
T cell proliferative responses upon stimulation with anti-TCR Ab or
MLR as well as in vivo primary response against staphylococcus
enterotoxin B administration were not different between T cells from
FcR-/- and wild-type mice. In addition,
the Ag presentation function of APCs from unimmunized
FcR-/- mice was normal. On the other hand,
Ab-deficient mice also revealed impaired T cell responses. These
results demonstrate that the defective T cell responses in
FcR-/- mice were due to impaired Ag
presentation during in vivo priming not to a defect in T cells.
Therefore, they suggest that the FcRs on APCs mediate efficient priming
of Th cell responses in vivo in an immune complex-dependent
manner.
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