Project/Area Number |
61570235
|
Research Category |
Grant-in-Aid for General Scientific Research (C)
|
Allocation Type | Single-year Grants |
Research Field |
Immunology
|
Research Institution | University of Tokyo |
Principal Investigator |
YANAGI Yusuke Research Associate, Faculty of Medicine, University of Tokyo, 医学部, 助手 (40182365)
|
Co-Investigator(Kenkyū-buntansha) |
YAGI Junji Research Associate, Faculty of Medicine, University of Tokyo, 医学部, 助手 (70182300)
|
Project Period (FY) |
1986 – 1987
|
Project Status |
Completed (Fiscal Year 1987)
|
Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1987: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1986: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
Keywords | T cell receptor / Antigen recognition / Suppressor T cell / 自己免疫疾患 |
Research Abstract |
1. The T cell receptor (TcR) is composed of <alpha> and <beta> chains. By transferring cloned and <beta> chain genes, it was established that this <alpha><beta> heterodimer is responsible for the dual specificity of T cells. However, it is still not known which amino acid residues are important in determining T cell specificities. In order to define important amino acid residues, we derived mutant T cell clones with altered specificities from an I-A^K reactive T cell clone, MS202. One mutant clone, E-3, was shown to respond to I-A^D and I-A^d as well as I-A^K. It seemed that this specificity change was due to the structural change of TcR in E-o as molecular weight of TcR was smaller in E-3 than in MS202. However, nucleotide sequences of TcR <alpha> and <beta> chain genes were identical between MS202 and E-3. It was found that E-3 has a defect in glycosylation. In addition, these two clones might express two kinds of TcR molecules with different chains. We are in a process of determining the cause of specificity change in E-3. 2. All murine suppressor T cell clones examined were shown to express TcR <alpha> and <beta> chain genes. We are now in a process of cloning genes specifically expressed in suppressor T cells using the subtraction hybridization. 3. The amount of mRNA coding for TcR <alpha> and <beta> chains was found to be almost constant whether T cells are activated by antigens or not. 4. The TcR <beta> chain gene of NZW mice seems to contribute to the autoimmunity in (NZB x NZW)F_1 mice.
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