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Released from T Cells Is Essential for Induction of Effector Macrophages in the Rejection Site1
Department of Cell Biology, Osaka Bioscience Institute, Suita, Osaka, Japan
Allografted Meth A tumor rejection is T cell dependent, but T cells
are inactive toward the allograft; rather, the main effector cells are
allograft-induced macrophages (AIM) with MHC haplotype specificity.
Here, we examined the role of T cells in the induction of AIM in the
rejection site. On day 4.5 after i.p. transplantation of Meth A
fibrosarcoma cells to C57BL/6 (B6) mice, we obtained a kind of
precursor of AIM (pro-AIM) from the transplantation site by an
enrichment technique involving adherence to serum-coated dishes. The
noncytotoxic pro-AIM-rich population put into a diffusion chamber
became cytotoxic against Meth A cells after 2 days in the peritoneal
cavity of an untreated B6 mouse. Similar activation of the chambered B6
pro-AIM-rich population occurred in IFN-
-/- B6 mice, whereas
there was no activation when chambers containing an IFN- -/-
mouse-derived pro-AIM-rich population were placed in normal or IFN-
-/- mice, suggesting that IFN- is involved in the activation.
RT-PCR experiments demonstrated that among bulk infiltrates T cells
were the major producer of IFN-; and most of the cells in a T
cell-eliminated pro-AIM population in a diffusion chamber kept for 2
days in a B6 mouse did not become AIM. Furthermore, IFN- -/- B6
mice could not reject allografted Meth A tumor cells, whereas the
grafts were rejected by i.p. injections of IFN- into the mutant
mice. These results indicate that IFN- released from
allograft-induced T cells is essential for both the activation of a
kind of pro-AIM to AIM in the transplantation site and the rejection of
an allografted tumor.
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