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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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Anti–IFN-γ reverses SEA-induced anergy. Treatment with anti–IFN-γ Ab increased CD4+ T cell recovery and viability after SEA treatment. (a) CD4+ T cells from SEA-treated and control AND mice were cultured with neutralizing concentration of anti–IFN-γ Ab (XMG1.2). Live cell  recovery on day 4 is shown. Cells recovered from above cultures were analyzed for live cell content. (b) Percentage of live cells as determined by F/S. (c)  Percentage of CD4+ cells that stained positively with PI. Gated populations of CD4+ cells are shown.
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Figure 6: Anti–IFN-γ reverses SEA-induced anergy. Treatment with anti–IFN-γ Ab increased CD4+ T cell recovery and viability after SEA treatment. (a) CD4+ T cells from SEA-treated and control AND mice were cultured with neutralizing concentration of anti–IFN-γ Ab (XMG1.2). Live cell recovery on day 4 is shown. Cells recovered from above cultures were analyzed for live cell content. (b) Percentage of live cells as determined by F/S. (c) Percentage of CD4+ cells that stained positively with PI. Gated populations of CD4+ cells are shown.

Mentions: Enriched populations of CD4+ cells from SEA-treated and control mice were stimulated in vitro with or without anti–IFN-γ (XMG1.2 at 10 μg/ml). After 48 and 96 h, the recovery of live CD4+ cells was determined (Fig. 6 a). In this representative experiment, treatment with anti–IFN-γ increased the live CD4+ recoveries in the SEA-treated groups to levels that were comparable with the controls, whereas in the absence of added Ab, no CD4+ cell growth occurred. Interestingly, anti–IFN-γ had comparatively little effect on the survival of control CD4+ cells from untreated animals.


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)

Anti–IFN-γ reverses SEA-induced anergy. Treatment with anti–IFN-γ Ab increased CD4+ T cell recovery and viability after SEA treatment. (a) CD4+ T cells from SEA-treated and control AND mice were cultured with neutralizing concentration of anti–IFN-γ Ab (XMG1.2). Live cell  recovery on day 4 is shown. Cells recovered from above cultures were analyzed for live cell content. (b) Percentage of live cells as determined by F/S. (c)  Percentage of CD4+ cells that stained positively with PI. Gated populations of CD4+ cells are shown.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 6: Anti–IFN-γ reverses SEA-induced anergy. Treatment with anti–IFN-γ Ab increased CD4+ T cell recovery and viability after SEA treatment. (a) CD4+ T cells from SEA-treated and control AND mice were cultured with neutralizing concentration of anti–IFN-γ Ab (XMG1.2). Live cell recovery on day 4 is shown. Cells recovered from above cultures were analyzed for live cell content. (b) Percentage of live cells as determined by F/S. (c) Percentage of CD4+ cells that stained positively with PI. Gated populations of CD4+ cells are shown.
Mentions: Enriched populations of CD4+ cells from SEA-treated and control mice were stimulated in vitro with or without anti–IFN-γ (XMG1.2 at 10 μg/ml). After 48 and 96 h, the recovery of live CD4+ cells was determined (Fig. 6 a). In this representative experiment, treatment with anti–IFN-γ increased the live CD4+ recoveries in the SEA-treated groups to levels that were comparable with the controls, whereas in the absence of added Ab, no CD4+ cell growth occurred. Interestingly, anti–IFN-γ had comparatively little effect on the survival of control CD4+ cells from untreated animals.

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