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Schepens Eye Research Institute, Department of Ophthalmology, Harvard Medical School, Boston, MA 02114
Macrophages incubated with OVA in the presence of
TGF-ß2 induce immune deviation in vivo (impaired
delayed hypersensitivity and IgG2a Ab production) when injected into
naive, syngeneic mice. OVA-specific TCR transgenic naive T cells
(DO11.10 T cells) produce Th1-type cytokines when stimulated in vitro
with OVA-pulsed peritoneal exudate cells (PEC), but if PEC are first
treated with TGF-ß2 and then pulsed with OVA, the T cells
secrete Th2-type cytokines instead. In this study, we investigated the
mechanisms that are involved in the modified Ag-presenting functions of
macrophages by TGF-ß2 pretreatment. We have found that:
1) TGF-ß2 impaired the capacity of PEC to produce IL-12
and to express CD40; 2) reduced CD40 expression on
TGF-ß2-treated PEC impaired IL-12 production when the
cells were cocultured with DO11.10 T cells; 3) the failure of
TGF-ß2-treated PEC to stimulate DO11.10 T cells to
secrete IFN-
was due to their impaired IL-12 production. From these
results, we conclude that TGF-ß2 treatment impairs the
ability of macrophages to produce IL-12 and to express CD40. As a
consequence, TGF-ß2-treated PEC fail to promote
development of pT cells toward the Th1 phenotype.
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