Skip to main content
. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: J Immunol. 2013 Aug 30;191(7):3838–3846. doi: 10.4049/jimmunol.1300524

Figure 4.

Figure 4

Activation of mTOR/p70 S6 kinase involved in the H. pylori mediated downregulation of B7-H2 expression. N87 cells were incubated with H. pylori 51B WT and cagA− strain. Cell were lysed after 5 min, 15 min, 30 min, 45 min and 60 min. Cell lysates from GEC exposed to H. pylori 51B WT and cagA− strain was analyzed for (A, C) phospho and (B, D) total p70 S6 kinase using Luminex bead array respectively. (E) GECs were treated with rapamycin (100 ng/ml) an inhibitor of mTOR/p70 S6 kinase pathway, (F) or with wortmannin (100 nM), AG-490 (100 ng/mL) and CAY10512 (10 μM) inhibitor for PI3K, STAT3 and NFκB pathway respectively, for 1 hour and then were infected with H. pylori. B7-H2 expression was analyzed using flow cytometry 24 hour later. Data expressed as a percentage of positive cells. Results represents as the mean ± SD (n=8); P=N.S. (Not significant); *P < .05.