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. Author manuscript; available in PMC: 2012 Aug 27.
Published in final edited form as: J Immunol. 2008 Dec 1;181(11):7721–7727. doi: 10.4049/jimmunol.181.11.7721

Figure 3. EphA2 agonist enhanced in vitro recognition of SLR20.A2 tumor cells by anti-EphA258-66 T cell clone 15/9 is proteasome-dependent.

Figure 3

SLR20.A2 cells were pre-treated with MG-132 (10 μM) or lactacystin (clasto-lactacystin β-lactone; 20 μM) or media for 3 hours, before being treated with 1 μg/ml MOPC-21 (control IgG), 1 μg/ml mAb208 or 0.1 μg/ml EphrinA1-Fc for an additional 3 hours. No toxicity was observed under any conditions. The effect of proteasomal inhibitors on agonist-induced degradation of EphA2 expression was confirmed by Western Blot (panel A.). After harvesting and washing the treated tumor cells extensively, these cells were used as targets for clone 15/9 (anti-EphA258-66) in IFN-γ ELISPOT assays (panel B) as outlined in Materials and Methods. Data from a representative experiment are reported as % control (mean +/− SD) T cell response to SLR20.A2 versus tumor cells treated with control IgG (i.e. MOPC21). *p < 0.05 vs. control IgG-treated tumor cells.