2002 Fiscal Year Final Research Report Summary
The development of specific immune regulatory drugs utilizing the structure and function of CD26
| Project/Area Number |
13557039
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
内科学一般
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MORIMOTO Chikao The Institute of Medical Science, Professor, 医科学研究所, 教授 (30119028)
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| Co-Investigator(Kenkyū-buntansha) |
KAWASAKI Hiroshi The Institute of Medical Science, 医科学研究所, 助手 (80280957)
HOSONO Osamu The Institute of Medical Science, 医科学研究所, 助手 (50190210)
TANAKA Hirotoshi The Institute of Medical Science, Associate Professor, 医科学研究所, 助教授 (00171794)
TANAKA Toshiaki Tray Industries, Inc., Group Leader (Researher), 基礎研究所, 主任研究員
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| Project Period (FY) |
2001 – 2002
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| Keywords | CD26 / costimulatory molecule / DPPIV / CD4 memory T cells / p2l^<ciple> / ERK / autoioimmune diseases |
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| Research Abstract |
CD26 is T cell costimulatory molecule with dipeptidyl peptidase IV (DPPIV) enzyme activity located in its extracellular region. The expression of CD26 is enhanced after activation of T cells, while it is preferentially expressed on a subset of CD4+ memory T cells in the resting state. In this paper, we demonstrate that binding of the soluble anti-CD26 monoclonal antibody (mAb) 1F7 inhibits human T-cell growth and proliferation in both CD26-transfected Jurkat T-cell lines and human T-cell clones by inducing G1/S arrest, which is associated with enhancement of p21Cip1 expression. This effect depends on the DPPIV enzyme activity of the CD26 molecule. Moreover, we show that expression of p21Cip1 after treatment with the anti-CD26 mAb 1F7 appears to be induced through activation of extracellular signal-regulated kinase (ERK) pathway. These data thus suggest that anti-CD26 treatment may have potential use in the clinical setting involving activated T cell dysregulation, including autoimmune disorders and graft-vs.-host disease.
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[Publications] Myake-Nishijima R, Iwata S, Saijo S, Kobayashi H, Kobayshi S, Souta-Kuribara A, Hosono O, Kawasaki H, Tanaka H, Ikeda E, Okada Y, Iwakura Y, Morimoto C: "Role of Crk-associated substrate lymphocyte type in pathophysiology of rheumatoid arthritis in tax transgemc mice and humans"Arthr.& Rheum. In press.
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