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. Author manuscript; available in PMC: 2009 Mar 27.
Published in final edited form as: Mol Ther. 2003 Jun;7(6):741–747. doi: 10.1016/S1525-0016(03)00120-5

FIG. 2.

FIG. 2

Viral therapy of intracranial melanoma increases both tumor- and viral-specific CTL activity. Effector lymphocytes were isolated from mock- and HSV-1 1716-treated tumor-bearing animals 20 days post-viral therapy and incubated for 3 days. Splenocytes were then examined for specific killing of target cells, either uninfected or infected tumor cells, using the Promega CytoTox96 nonradioactive cytotoxicity assay. (A) A tumor-specific CTL response develops following viral therapy. Splenocytes isolated from either mock-treated tumor-bearing mice (square) or HSV-1 1716-treated tumor-bearing mice (triangle) were examined for specific killing of target uninfected tumor cells. (B) A viral-specific CTL response develops following viral therapy. Splenocytes isolated from HSV-1 1716-treated tumor-bearing animals were examined for specific killing of target cells, either uninfected (square) or HSV-1 infected (triangle) tumor cells. No response is seen toward the control targets, including H2-matched cells (F4) (circle), H2-unmatched melanoma (S91 and HP) (diamond and plus sign), or Hve-expressing CHO cells (M1A, M3A, and CHO) (x, dash, and asterisk). Each line represents the average percentage of specific killing as a function of maximum LDH release at various E/T ratios for N = 5 mice per group.