Figure 6
Figure 6. LPS- but not CD40L-matured LXR agonist–treated DCs fail to induce IS formation. Immature DCs (iDCs) were differentiated for 7 days and left untreated (control) or treated from day 2 on with 2 μM of the LXR agonist T0901317 (T09). Mature DCs were obtained from iDCs by incubation with LPS or CD40L for the last 2 days. Mature DCs were pulsed with superantigen for 30 minutes and incubated with Jurkat T cells for an additional 30 minutes. CD3ϵ and PKCθ relocalization was visualized by indirect immunofluorescence. Typical examples of conjugates, negative (left) or positive (right) for relocalization of CD3ϵ and PKCθ, are shown. Bar represents 10 μm. The diagram shows the percentage of conjugates counted positive for CD3ϵ and PKCθ relocalization in means ± SEM of 4 independent experiments. Significance versus untreated mDCs: *P ≤ .05.

LPS- but not CD40L-matured LXR agonist–treated DCs fail to induce IS formation. Immature DCs (iDCs) were differentiated for 7 days and left untreated (control) or treated from day 2 on with 2 μM of the LXR agonist T0901317 (T09). Mature DCs were obtained from iDCs by incubation with LPS or CD40L for the last 2 days. Mature DCs were pulsed with superantigen for 30 minutes and incubated with Jurkat T cells for an additional 30 minutes. CD3ϵ and PKCθ relocalization was visualized by indirect immunofluorescence. Typical examples of conjugates, negative (left) or positive (right) for relocalization of CD3ϵ and PKCθ, are shown. Bar represents 10 μm. The diagram shows the percentage of conjugates counted positive for CD3ϵ and PKCθ relocalization in means ± SEM of 4 independent experiments. Significance versus untreated mDCs: *P ≤ .05.

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