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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Hum Immunol. 2013 Apr 18;74(7):842–848. doi: 10.1016/j.humimm.2013.04.002

Fig. 3.

Fig. 3

Porcine CTLA-4-L97M mutant obtained weak binding to human CD80. (A) Flow cytometry binding analysis of porcine CTLA-4 (left panel) and porcine CTLA-4-L97M mutant (right panel) to the human CD80-expressing acute myelogenous leukemia cell line. PE-SA only; biotinylated protein control (pCD3εγ) [10]; isotype control [biotinylated mouse (BALB/c) IgG1, κ, clone# MOPC-21, Biolegend] were included. (B) Bar graph presentation of the MFI from flow cytometry binding analysis data from (A). Different concentrations of biotinylated pCD3εγ were used as non-specific fluorescence control. Error bars are included based on the calculated standard deviation. The pCTLA-4-L97M mutant conferred a weak but significant ability to bind to human CD80 compared to the pCTLA-4-WT, p < 0.05. (C) CD80 blocking analysis by flow cytometry for porcine CTLA-4 (left panel) and porcine CTLA-4-L97M mutant (right panel) with anti-human CD80 mAb (clone 2D10) to the human CD80-expressing acute myelogenous leukemia cell line. The concentration of the competitor is indicated. All figures in (A)–(C) are representatives of multiple individual experiments.