Antigenic drift as a mechanism for tumor evasion of destruction by cytolytic T lymphocytes
J. Clin. Invest. Xue-Feng Bai, et al. 111:1487 doi:10.1172/JCI17656 [Go to this article.]

Figure 7
In adoptive therapy, TCR α chain–transgenic T cells mounted a robust CTL response against the P1A35-43 epitope presented by H-2L^d and caused transient rejection of large established tumors. (a) Expression of P1CTL TCR α chain on more than 90% of T cells, as revealed by coexpression of the transgenic Vα8 chain and CD3 or CD8. A significant (although small) proportion of CD8 T cells reacted specifically to H-2L^d:P1A complex. (b) Adoptive transfer therapy of mice with large tumor burdens using spleen cells from either TCR α chain–transgenic mice or their wild-type, nontransgenic (Ntg) littermates. RAG-2^–/– BALB/c mice were transplanted with 5 × 10⁶ J558-Neo tumor cells. Once tumors were greater than 1.5 cm in diameter, unprimed spleen cells from either wild-type or transgenic littermates were injected intravenously. Tumor growth was monitored with calipers. Data show average tumor diameter of five mice per group. ^†The time of sacrifice. **Significantly different from nontransgenic (P ≤ 0.01) as determined by Student t test. (c) Robust CTL response in mice that received transgenic T cells. At 4–5 weeks after adoptive transfer, spleen cells of recipient mice were stained with anti-CD8 in conjunction with H-2L^d loaded with either control or P1A peptides. Three independent experiments revealed that 10–70% of CD8 T cells were capable of binding the H-2L^d:P1A complex.