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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: J Immunother. 2013 Feb;36(2):112–123. doi: 10.1097/CJI.0b013e3182811ce9

Figure 1. K562-derived aAPC (clone #4) sustains proliferation of CAR+ T cells.

Figure 1

(a) Phenotype of aAPC. Flow cytometry analyses revealed the expression of proteins derived from (i) the introduced transgenes CD19, CD64, CD86, and CD137L and (ii) membrane-bound IL-15 (mIL-15) co-expressed via IRES with EGFP. (b) Stability of the expression of introduced transgenes aAPC by flow cytometry. (c) CD19-specific CAR and CD3 expression and lack of CD32 expression on genetically modified and propagated T cells. Shown here are CD19-specific CAR and CD3 expression on Day 28 after electroporation. Although on Day 1, CAR expression was from episomal and integrated plasmids, at Day 28, the expression of this CAR transgene was from the integrated plasmid only. On Day 28, there was negligible (1%) expression of CD32, which was consistent with the loss of the aAPC which homogenously express endogenous CD32. (d) Numeric expansion of CAR+ and CD3+ T cells upon recursive additions of γ-irradiated aAPC. Upward arrows indicate additions of aAPC to culture. T cells were enumerated every 7 days, and viable cells were counted based on Trypan blue exclusion.