Abstract

Purified splenic T cells from C3H/HeN mice primed with immunosuppressive fraction (ISF) from A. actinomycetemcomitans were adoptively transferred to syngeneic mice with SRBC. The transfer of splenic T cells from mice, primed with various amounts of ISF for 6 days, resulted in the dose-dependent inhibition of IgM anti-sheep red blood cells (SRBC) plaque-forming cells (PFC) compared with normal and BSA-primed splenic T cells. Furthermore, the transfer of T cells from mice primed with 100 micrograms of ISF for 6 days to syngeneic and CD4-depleted mice caused the highest inhibition. Immune suppression did not depend on the B cell population in spleen from donor mice primed with ISF, nor on haplotypes as recipient. The immunosuppressive function of these ISF-primed T cells was abrogated by 1000 rad irradiation. Splenic T cells from ISF-treated mice could suppress the T cell-dependent proliferative responses of cocultured normal spleen cells in vitro. Analysis of T cell subsets of spleen cells from ISF-treated mice showed that the suppressor cell is susceptible to treatment with anti-CD8 and complement (C). ISF-sensitized suppressor T cells also suppressed secondary IgG anti-SRBC-PFC response after immunization with SRBC in vivo depending on sensitized periods induced by ISF. Treatment of T cells from mice which primed with ISF for 8 days, with goat anti-mouse CD8 antibody and C abrogated their suppressive effects, and secondary IgG response occurred. These results indicate that the adoptive transfer of ISF-induced T cells, which increased suppressor function, caused the perfect blocking of immune response, allowing promotion of secondary infection.

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