| Project/Area Number |
09671863
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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 |
Morphological basic dentistry
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| Research Institution | Ohu University School |
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Principal Investigator |
NITTA Toshinasa Ohu Univ., Oral microbiology, Professor, 歯学部, 教授 (20104317)
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| Co-Investigator(Kenkyū-buntansha) |
SHOJI Hiroe Ohu Univ., Oral microbiology, Research assistant, 歯学部, 助手 (40285705)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | lipid A / memory T cell / macrophage-independent / NK cell / CD28 / Th2細胞 / CD44抗原 |
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| Research Abstract |
Highly purified T cells of mice that have been primed in vivo with horse red blood cells (HRBC) and lipid A, but not with HRBC alone, can proliferate in vitro in response to HRBC or anti-alphabeta T cell receptor (TCR) antibody without macrophages. Mechanism of the proliferation without macrophages was investigated. Purified T cells were obtained from the peritoneal exudate cells (PEC) and the cell proliferation was assessed by [^3H]-thymidine (TdR) incorporation into the cultured T cells in response to HRBC or anti-alphabeta TCR antibody. The proliferation of T cells [T(HRBC+lipid A)] that had been prepared from the PEC of the mice primed with HRBC and lipid A increased dose-dependently to these stimulants, but T cells [T(HRBC)] prepared from PEC mice primed with HRBC showed little or no proliferation in response to them. The expression pattern of a memory cell marker, CD44, on the cell surface of T(HRBC+lipid A) was obviously different from that on T(HRBC). The proliferation of T(HRBC+lipid A) was suppressed when the cells were cultured in the wells coated with hyaluronate, a ligand for CD44, or cultured after a previous treatment with anti-CD44 (IgG2a) and anti-IgG2a antibodies. In contrast, the proliferation of T(HRBC) was up-regulated in culture under the same condition. Proliferative responses of T(HRBC-i-lipid A) to anti-alphabeta TCR antibody were enhanced in the wells coated with anti-CD28 antibody. These findings indicate that the proliferation of T(HRBC+lipid A) was riot only supported by a stimulation of TCR but also regulated by the other stimulation via ligand such as for CD44 and CD28. The proliferation of T(HRBC+lipid A) was abolished when the cells had been pretreated with AsGM1 antibody or anti-CD8O antibody and C.These findings indicate that the in vivo priming of mice with HRBC and lipid A generates the memory T cell population that is capable of proliferating without help of macrophages, but with NK cells, when stimulated their TCR.
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