Tumor immune escape and the role of CD4 regulatory T cells

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The involvement of two phenotypically different regulatory T cells in tumor growth was investigated. Treatment of BALB/c mice with anti-CD25 mAb (PC61), but not anti-CD4 mAb (GK1.5) before RL male 1 or Meth A inoculation caused the tumor rejection. On the other hand, treatment of BALB/c mice with anti-CD4 mAb (GK1.5) but not anti-CD25 mAb (PC61) on day 6 after inoculation of the same tumors caused rejection. The findings suggested that CD4^+CD25^+ T cells downregulated the rejection response in the early stage of tumor growth. On the other hand, CD4^+CD25^- T cells downregulated the tumor rejection response in the following stage. Both CD4^+CD25^+ and CD4^+CD25^- T cells appeared to inhibit the efficient generation of CTL. Treatment of the mice with anti-CD25 mAb (PC61) before tumor inoculation did not result in continuous tumor growth also suggested that CD4^+CD25^- regulatory T cells did not appear following CD25-depletion. The present study also demonstrated that the treatment of BALB/c mice with anti-CD25 mAb (PC61) at 4 or 6 weeks after 3-methylcholanthrene (3-MC) inoculation retarded tumor occurrence.Furthermore, CD4^+CD25^+ regulatory cells appeared to be involved in tumorgenesis of p53^<-/-> mice. The findings indicated that CD4^+CD^25 regulatory cells are involved in tumorgenesis of established tumor and also tumorgenesis by methylcholanthrene and in p53^<-/-> mice.