Figure 4
IL-2 inhibits Th17 differentiation of TRAF6-deficient CD4+ T cells. CD4+ T cells were isolated from TRAF6-ΔT and control mice and stimulated under optimal Th17-polarizing conditions for 4 days (Th17). Neutralizing antibody against murine IL-2 (S4B6, 10 μg/mL) plus blocking antibody against CD25 (3C7, 10 μg/mL) or recombinant human IL-2 (100 U/mL) were added to the cultures as indicated. Numbers in flow cytometry plots indicate percentages of IL-17–expressing CD4+ T cells. Dot plot panels of conditions with added recombinant IL-2 (+ IL-2) are from a separate experiment. Bottom panels show the percentages of IL-17–positive cells from separate experiments using triplicate cultures per experimental condition. Values on top of bars indicate fold increase relative to cells differentiated in regular Th17 conditions. Experiments were repeated twice with similar results.*P < .01, **P < .05, ***P > .1.

IL-2 inhibits Th17 differentiation of TRAF6-deficient CD4+ T cells. CD4+ T cells were isolated from TRAF6-ΔT and control mice and stimulated under optimal Th17-polarizing conditions for 4 days (Th17). Neutralizing antibody against murine IL-2 (S4B6, 10 μg/mL) plus blocking antibody against CD25 (3C7, 10 μg/mL) or recombinant human IL-2 (100 U/mL) were added to the cultures as indicated. Numbers in flow cytometry plots indicate percentages of IL-17–expressing CD4+ T cells. Dot plot panels of conditions with added recombinant IL-2 (+ IL-2) are from a separate experiment. Bottom panels show the percentages of IL-17–positive cells from separate experiments using triplicate cultures per experimental condition. Values on top of bars indicate fold increase relative to cells differentiated in regular Th17 conditions. Experiments were repeated twice with similar results.*P < .01, **P < .05, ***P > .1.

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