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Adoptive transfer of suppressor T cells induced by Actinobacillus actinomycetemcomitans regulates immune response
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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 μg 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.
Title: Adoptive transfer of suppressor T cells induced by Actinobacillus actinomycetemcomitans regulates immune response
Description:
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 μg 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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