Skip to main content
. 2015 Dec 4;6(41):43230–43243. doi: 10.18632/oncotarget.6462

Figure 1. Inflammation of primary human myoblasts results in an upregulation of surface expression, but reduced shedding of NKG2D ligands.

Figure 1

A. The surface expression of NKG2D ligands on primary human myoblasts was assessed under different inflammatory conditions (IFNγ: 1000 U/ml and/or TNFα: 1000 U/ml for 48 h). Histograms show the fluorescence intensity for the NKG2D ligands of unstimulated (grey, unstim) and inflamed (black) myoblasts or the isotype control (dashed line), one representative example is shown (n = 5) and mean fluorescence intensity (MFI) of each population is depicted. B. Soluble MICA (sMICA) ELISA of human myoblast cell culture supernatants. Myoblasts were treated with IFNγ (1000 U/ml) and/or TNFα (1000 U/ml) for 48 h (n = 4). C. Relative expression of ADAM (A Disintegrin and Metalloproteinase) peptidase proteins 9, 10 and 17, responsible for NKG2D ligand shedding, under basal and inflammatory conditions in human myoblasts assessed by RT-PCR (n = 4). * p < 0.05, ns = not significant.