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Transferable anergy: superantigen treatment induces CD4+ T cell tolerance that is reversible and requires CD4-CD8- cells and interferon gamma.

Cauley LS, Cauley KA, Shub F, Huston G, Swain SL - J. Exp. Med. (1997)

Bottom Line: Bacterial superantigens induce peripheral unresponsiveness in CD4+ T cell populations that express appropriate Vbeta chains.However, when the SEA-treated CD4+ cells were completely purified away from all other contaminating cells, they regained the ability to proliferate and secrete cytokines.Further analysis demonstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.

View Article: PubMed Central - PubMed

Affiliation: Trudeau Institute, Saranac Lake, New York 12983, USA.

ABSTRACT
Bacterial superantigens induce peripheral unresponsiveness in CD4+ T cell populations that express appropriate Vbeta chains. We have used Vbeta3/Valpha11 T cell receptor transgenic (Tg) mice and the Vbeta3-specific superantigen staphylococcal enterotoxin A (SEA) to further investigate the mechanisms that contribute to such unresponsiveness. As in other models, in vivo exposure to SEA rendered the Tg CD4+ cells unresponsive to subsequent restimulation in vitro with antigen or mitogens. However, when the SEA-treated CD4+ cells were completely purified away from all other contaminating cells, they regained the ability to proliferate and secrete cytokines. Moreover, enriched CD4-CD8- cells from the SEA-treated mice suppressed the responses of fresh control CD4+ cells in mixed cultures indicating that the apparent "anergy" was both transferable and reversible. Further analysis demonstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.

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rIFN-γ does not  suppress CD4+ cells from untreated AND mice. Naive CD4+  T cells were stimulated with  APCs and PCCF in the presence  of increasing concentrations of  rIFN-γ. Live CD4+ T cell recovery on day 4 is shown. Anti– IFN-γ also did not significantly alter live cell recovery (not shown).
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Figure 10: rIFN-γ does not suppress CD4+ cells from untreated AND mice. Naive CD4+ T cells were stimulated with APCs and PCCF in the presence of increasing concentrations of rIFN-γ. Live CD4+ T cell recovery on day 4 is shown. Anti– IFN-γ also did not significantly alter live cell recovery (not shown).

Mentions: We also investigated whether rIFN-γ would suppress effector cell generation by naive CD4+ cells. However, even additions of >1,000 U/ml of exogenous rIFN-γ, a high dose compared with the small amounts (∼200 U/ml) detected in the suppressed cultures (Fig. 1), did not cause any significant reduction in the size of the live cell population generated over 4 d (Fig. 10). Thus, although IFN-γ was clearly required for the SEA-induced anergy, it was not likely to be entirely responsible for the loss of CD4+ cell function.


Transferable anergy: superantigen treatment induces CD4+ T cell tolerance that is reversible and requires CD4-CD8- cells and interferon gamma.

Cauley LS, Cauley KA, Shub F, Huston G, Swain SL - J. Exp. Med. (1997)

rIFN-γ does not  suppress CD4+ cells from untreated AND mice. Naive CD4+  T cells were stimulated with  APCs and PCCF in the presence  of increasing concentrations of  rIFN-γ. Live CD4+ T cell recovery on day 4 is shown. Anti– IFN-γ also did not significantly alter live cell recovery (not shown).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2198967&req=5

Figure 10: rIFN-γ does not suppress CD4+ cells from untreated AND mice. Naive CD4+ T cells were stimulated with APCs and PCCF in the presence of increasing concentrations of rIFN-γ. Live CD4+ T cell recovery on day 4 is shown. Anti– IFN-γ also did not significantly alter live cell recovery (not shown).
Mentions: We also investigated whether rIFN-γ would suppress effector cell generation by naive CD4+ cells. However, even additions of >1,000 U/ml of exogenous rIFN-γ, a high dose compared with the small amounts (∼200 U/ml) detected in the suppressed cultures (Fig. 1), did not cause any significant reduction in the size of the live cell population generated over 4 d (Fig. 10). Thus, although IFN-γ was clearly required for the SEA-induced anergy, it was not likely to be entirely responsible for the loss of CD4+ cell function.

Bottom Line: Bacterial superantigens induce peripheral unresponsiveness in CD4+ T cell populations that express appropriate Vbeta chains.However, when the SEA-treated CD4+ cells were completely purified away from all other contaminating cells, they regained the ability to proliferate and secrete cytokines.Further analysis demonstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.

View Article: PubMed Central - PubMed

Affiliation: Trudeau Institute, Saranac Lake, New York 12983, USA.

ABSTRACT
Bacterial superantigens induce peripheral unresponsiveness in CD4+ T cell populations that express appropriate Vbeta chains. We have used Vbeta3/Valpha11 T cell receptor transgenic (Tg) mice and the Vbeta3-specific superantigen staphylococcal enterotoxin A (SEA) to further investigate the mechanisms that contribute to such unresponsiveness. As in other models, in vivo exposure to SEA rendered the Tg CD4+ cells unresponsive to subsequent restimulation in vitro with antigen or mitogens. However, when the SEA-treated CD4+ cells were completely purified away from all other contaminating cells, they regained the ability to proliferate and secrete cytokines. Moreover, enriched CD4-CD8- cells from the SEA-treated mice suppressed the responses of fresh control CD4+ cells in mixed cultures indicating that the apparent "anergy" was both transferable and reversible. Further analysis demonstrated that interferon gamma, but not the Fas receptor, played a critical role in the suppression.

Show MeSH
Related in: MedlinePlus