| Project/Area Number |
13670319
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
NAKAYAMA Eiichi Okayama UniversityGraduate School of Medicine and Dentistry, Professor, 大学院・医歯学総合研究科, 教授 (60180428)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | immune surveillance / regulatory T cells / murine tumors / tumor growth / CTL / methylcholanthrene / p53^<- / -> / CD25 |
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| Research Abstract |
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.
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