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. 2013 Jan 24;121(13):2512–2521. doi: 10.1182/blood-2012-08-449025

Figure 4.

Figure 4

T and NK cells mediate regression of tumor cells in blood. (A) Percentage of CD62LlowCD3+CD4+, CD62LlowCD3+CD8+ T cells and MHC class I (H-2Kb and H-2Db) levels on B220low cells in the blood of preregression and postregression Eμ-myc mice and WT mice at <41 days of age (bold lines). Staining of MHC class I expression was compared with WT B220low cells (dashed line) or isotype controls (filled histogram). P values are indicated as HP < .009 and HHP = .001. (B-G) To determine effector mechanisms of tumor regression in vivo, Eμ-myc mice at 34 ± 2 days of age were treated with (B,C) anti-CD4 (500 μg/mouse), anti-CD8 (250 μg/mouse), and anti-NK1.1 (500 μg/mouse) antibodies. In some experiments mice were treated with anti-CD4 and CD8 antibodies (D), anti-CD4 (E), anti-CD8 (F), or anti-NK1.1 (G). Tumor load in the blood was determined by flow cytometry at 34 days of age (preregression) and during regression at 41 (B-F), 48 (B-F), and 55 days of age (B,C,D,G). Because T-cell depletion influences the percentage of tumor load in the blood, tumor load at 41 days of age was compared with the tumor load at 48 and 55 days of age. (C) The number of B220low cells in blood was determined as outlined in Figure 1C. Graphs represent the combined data from 2 independent experiments. ctrl, control; d, day.