Figure 2.
Figure 2. CXCR3 agonists stimulate activation of p44/p42 MAPK in T lymphocytes. (A-B) Activated IL-2–expanded blood T cells were incubated for 15 minutes with various concentrations of CXCL11 (A), CXCL10 (B), or CXCL9 (B) before lysis of the cells. Phosphorylation of p44/p42 MAPK was determined by Western blot analysis using specific anti–phosho-p44/p42 (P-p44/p42) antibodies. Phosphorylation was quantified by chemiluminescence and corrected for total MAPK (T-p44/p42) expression on stripped blots. (C-E) Involvement of Raf-MEK–(C), Gi- (D), and PI3K–signaling pathway (E) in CXCL11-induced p44/p42 MAPK phosphorylation. T cells were grown in serum-free medium in the presence of U0126 (10 μM, 30 minutes; C), PTX (100 ng/mL, 48 h; D), or wortmannin (wort) (100 nM, 30 minutes; E), and exposed to CXCL11 (15 minutes, 30 nM) before lysis and Western blot analysis. A representative experiment of at least 2 independent experiments is shown.

CXCR3 agonists stimulate activation of p44/p42 MAPK in T lymphocytes. (A-B) Activated IL-2–expanded blood T cells were incubated for 15 minutes with various concentrations of CXCL11 (A), CXCL10 (B), or CXCL9 (B) before lysis of the cells. Phosphorylation of p44/p42 MAPK was determined by Western blot analysis using specific anti–phosho-p44/p42 (P-p44/p42) antibodies. Phosphorylation was quantified by chemiluminescence and corrected for total MAPK (T-p44/p42) expression on stripped blots. (C-E) Involvement of Raf-MEK–(C), Gi- (D), and PI3K–signaling pathway (E) in CXCL11-induced p44/p42 MAPK phosphorylation. T cells were grown in serum-free medium in the presence of U0126 (10 μM, 30 minutes; C), PTX (100 ng/mL, 48 h; D), or wortmannin (wort) (100 nM, 30 minutes; E), and exposed to CXCL11 (15 minutes, 30 nM) before lysis and Western blot analysis. A representative experiment of at least 2 independent experiments is shown.

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