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Tumor escape mechanisms in leukemia are not well defined. To dissect immunological mechanisms responsible for immune tolerance toward leukemia, we established a murine model system allowing clonotypic analysis of leukemia-specific CD4 T cells recognizing ovalbumin (OVA). Upon i.v. injection of genetically engineered leukemia cells, dendritic cells (DCs) engulfed, processed and presented OVA to OVA-specific CD4 T cells. Consequently, leukemia-specific T cells were primed in vivo as shown by expression of activation markers and proliferative responses. However, in spite of detectable CD4 T cell responses in vitro and in vivo, no effective anti-leukemia immunity was established. In contrast, adoptively transferred DO11.10 T cells that were primed ex vivo mediated effective antitumor immunity. Furthermore, ex vivo primed DO11.10 T cells showed high expression of Th1 cytokines (interferon-gamma, tumor necrosis factor-alpha and interleukin-2) whereas in vivo primed OVA-specific CD4 T cells showed incomplete differentiation (proliferation without cytokine production). We conclude that activated T cells lacking effector function develop through incomplete differentiation in leukemia-bearing mice. Thus, priming conditions of leukemia-specific CD4 T cells critically determines the balance between immunity or tolerance toward leukemia.

Original publication




Journal article



Publication Date





2070 - 2079


Animals, CD4-Positive T-Lymphocytes, Cell Proliferation, Dendritic Cells, Disease Models, Animal, Female, Flow Cytometry, Fusion Proteins, bcr-abl, Humans, Immune Tolerance, Immunity, Interferon-gamma, Leukemia, Experimental, Mice, Mice, Inbred BALB C, Ovalbumin, Precursor Cell Lymphoblastic Leukemia-Lymphoma, T-Lymphocytes, Regulatory, Th1 Cells, Thymidine, Tumor Cells, Cultured