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The analysis of TLR and TCR Vβ repertoire which would determinate and innate immunity

Research Project

Project/Area Number 16591277
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field General surgery
Research InstitutionTokyo Women's Medical University

Principal Investigator

ARUGA Atsushi  Tokyo Women's Medical University, Graduate School of Medical Science, Professor (40221056)

Project Period (FY) 2004 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2004: ¥1,500,000 (Direct Cost: ¥1,500,000)
KeywordsToll like receptor / TCR Vβ / innate immunity / γδ T cell / dendritic cell
Research Abstract

An innate immunity against bacteria, virus and abnormal cells is carried on the macrophage, dendritic cell, neutrophil, NK cell and γδT cell which belong to white blood cell. They have the receptor against each antigen named toll-like receptor (TLR). In human system, the expressions of TLR1~9 are not equal and that make the differences of cytokine release from the cells when their TLR meet the ligand. These differences of TLR expression would decide the clinical progress in the patients with infection or cancer. As well as the cytokine release, the signal transduction from TLR would activate MyD88 and NF-kB gene, and induce the expression of cell surface molecules which could activate the NK cells or γδT cells.
The analysis of TCR Vβ repertoire was also done in the same patients. There were differences in the populations of each TCR Vβ. However, any correlation between TLR expression and TCR Vβ repertoire were not seen in this study. Especially, it was suggested that TCR Vβ repertoire would make an important role to induce a required immunity.
From now on, the analysis of TLR expression and TCR Vβ repertoire in the patients of cancer or infection will be needed to assess their immunological function to develop a new strategy for cancer and infection.

Report

(4 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report
  • 2004 Annual Research Report

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Published: 2004-04-01   Modified: 2016-04-21  

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