Figure 4.
Figure 4. The blockade of CD137-CD137L interactions suppresses phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK, and expression of Bcl-2 and p-Bad. (A) Western blotting analysis was conducted on the lysates of Hut78 and MyLa cells treated with anti-CD137L–neutralizing antibody (5 μg/mL) or isotype control for 0, 6, 12, or 24 hours. Phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK, and expression of Bcl-2 and p-Bad were measured. (B-C) Hut78, MyLa cells, and PBMCs from 4 SS patients as well as 3 healthy controls were treated with anti-CD137L–neutralizing antibody (5 μg/mL) or isotype control for 24 hours. Expression levels of p-AKT, p-ERK1/2, p-p38 MAPK, p-JNK, Bcl-2, and p-Bad were determined by intracellular flow cytometry in Hut78, MyLa cells (B), CD4+CD7− T cells from PBMCs of SS patients and CD4+ T cells from healthy controls (C). The MFI expression was normalized against the MFI expression of isotype-treated cells. Representative results are shown. *P < .05, **P < .01

The blockade of CD137-CD137L interactions suppresses phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK, and expression of Bcl-2 and p-Bad. (A) Western blotting analysis was conducted on the lysates of Hut78 and MyLa cells treated with anti-CD137L–neutralizing antibody (5 μg/mL) or isotype control for 0, 6, 12, or 24 hours. Phosphorylation of AKT, ERK1/2, p38 MAPK, and JNK, and expression of Bcl-2 and p-Bad were measured. (B-C) Hut78, MyLa cells, and PBMCs from 4 SS patients as well as 3 healthy controls were treated with anti-CD137L–neutralizing antibody (5 μg/mL) or isotype control for 24 hours. Expression levels of p-AKT, p-ERK1/2, p-p38 MAPK, p-JNK, Bcl-2, and p-Bad were determined by intracellular flow cytometry in Hut78, MyLa cells (B), CD4+CD7 T cells from PBMCs of SS patients and CD4+ T cells from healthy controls (C). The MFI expression was normalized against the MFI expression of isotype-treated cells. Representative results are shown. *P < .05, **P < .01

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