Figure 5
CCL21-mediated costimulation and signaling pathways in DOCK2-deficient T cells. (A) 2B4 TCR-tg CD4+ T cells were cocultured with MCC88-103-pulsed irradiated splenocytes in the presence or absence of CCL21 (100 nM). T-cell activation was determined as described in “Proliferation assays.” Proliferation of TCR-tg DOCK2+/− and DOCK2−/− 2B4 TCR-tg T cells after 48 hours is shown. Numbers indicate fold increase of proliferation in the presence of CCL21. Data are pooled from 3 independent experiments. *P < .05 compared with “no chemokine.” (B) Control and DOCK2−/− 2B4 TCR-tg T cells were stimulated as in Figure 3 and analyzed for Rac-GTP formation. One representative experiment of 2 is shown. (C) Control and DOCK2−/− 2B4 TCR-tg T cells were stimulated as in Figure 3 and analyzed for phosphorylation of ERK1/2 and Ras-GTP formation. One representative experiment of 3 is shown.

CCL21-mediated costimulation and signaling pathways in DOCK2-deficient T cells. (A) 2B4 TCR-tg CD4+ T cells were cocultured with MCC88-103-pulsed irradiated splenocytes in the presence or absence of CCL21 (100 nM). T-cell activation was determined as described in “Proliferation assays.” Proliferation of TCR-tg DOCK2+/− and DOCK2−/− 2B4 TCR-tg T cells after 48 hours is shown. Numbers indicate fold increase of proliferation in the presence of CCL21. Data are pooled from 3 independent experiments. *P < .05 compared with “no chemokine.” (B) Control and DOCK2−/− 2B4 TCR-tg T cells were stimulated as in Figure 3 and analyzed for Rac-GTP formation. One representative experiment of 2 is shown. (C) Control and DOCK2−/− 2B4 TCR-tg T cells were stimulated as in Figure 3 and analyzed for phosphorylation of ERK1/2 and Ras-GTP formation. One representative experiment of 3 is shown.

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