Figure 4
Figure 4. Increased SOCS3 and inhibition of STAT5 phosphorylation in CMV-MoDCs. (A-B) Mock-infected (Med), HCMV-infected (CMV), or IL-6–treated (50 ng/mL) monocytes were differentiated by culture with GM-CSF and IL-13 for 5 days. Alternatively, medium (NT), or neutralizing Ab against IL-6 receptor (αIL-6R; 15 μg/mL) or isotype Ab (iso; 15 μg/mL) was added to infected cells during differentiation. SOCS1, SOCS3, and β-actin mRNAs were analyzed by RT-PCR. (C-D) Total and phosphorylated STAT5 protein (pSTAT5) were assessed by Western blotting of mock-infected (Med) and HCMV-infected (CMV) cells. Cells were transfected with SOCS1, SOCS3, and control small interfering RNA (siRNA; Ctrl) as indicated. β-actin was used as control. The histograms below RT-PCR (A-B) and Western blots (C-D) represent the quantification of 3 independent experiments.

Increased SOCS3 and inhibition of STAT5 phosphorylation in CMV-MoDCs. (A-B) Mock-infected (Med), HCMV-infected (CMV), or IL-6–treated (50 ng/mL) monocytes were differentiated by culture with GM-CSF and IL-13 for 5 days. Alternatively, medium (NT), or neutralizing Ab against IL-6 receptor (αIL-6R; 15 μg/mL) or isotype Ab (iso; 15 μg/mL) was added to infected cells during differentiation. SOCS1, SOCS3, and β-actin mRNAs were analyzed by RT-PCR. (C-D) Total and phosphorylated STAT5 protein (pSTAT5) were assessed by Western blotting of mock-infected (Med) and HCMV-infected (CMV) cells. Cells were transfected with SOCS1, SOCS3, and control small interfering RNA (siRNA; Ctrl) as indicated. β-actin was used as control. The histograms below RT-PCR (A-B) and Western blots (C-D) represent the quantification of 3 independent experiments.

Close Modal

or Create an Account

Close Modal
Close Modal