In the recent past, it has repeatedly been reported that CD4 cells play an important role in the immunology of chronic myeloid leukaemia. It was therefore of interest to test their activity in an animal model using bcr-abl-transformed cells. BALB/c mice were four times immunized with a DNA vaccine carrying the bcr-abl fusion gene. Two weeks after the last vaccine dose, the animals were challenged with syngeneic bcr-abl-transformed 12B1 cells which form solid tumors after subcutaneous administration. At the time of challenge, animals were treated with antibodies against the CD8+ T cells or CD4+ T cells. The efficacy of the depletion was monitored and found highly effective. All nonimmunized animals developed tumors. All animals untreated with the antibodies as well as those in which CD8+ T cells had been depleted, were fully protected against the challenge. On the other hand, almost all mice treated with anti-CD4+ antibody developed tumors. These results strongly suggested that the CD4+ T cells acted as effectors in the present system. 1. Introduction It is generally accepted that specifically activated CD8+ T cells play the most important role in immunological tumor rejection and a great majority of immunotherapeutic studies have been focusing on them. In the recent past, it has repeatedly been demonstrated that the CD4+ T cell response is polyfunctional and there has been growing evidence that a subpopulation of CD4+ T cells can mediate an efficient antitumor activity in some systems (for review see [1, 2]). Activated CD4+ T cells may partner with many different types of host cells to clear the tumor indirectly by secretion of vast array of cytokines. These cytokines react with and activate distinct classes of cells including macrophages, eosinophils, NK cells, and B cells and can induce antitumor effect independent of CD8+ T cells [3]. Evidence of direct cytotoxic role for CD4+ T cells has also been presented [4, 5]. Cytotoxic CD4+ T cells have been detected in peripheral blood of subjects suffering from various diseases such as those caused by viruses (HIV, CMV, and EBV) (for review see [6]) and chronic inflammatory diseases as rheumatoid arthritis [7] and B-cell chronic lymphocytic leukaemia [8]. It has been shown that their cytotoxic effect has been based on perforin-dependent pathway [9] and/or on the Fas-FasL-mediated apoptosis [10], and it has been suggested that the lytic activity of CD4+ T cells is likely HLA class II restricted, at least in some instances. In our previous study, we have shown that it is possible to induce solid immunity
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