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2018 Fiscal Year Final Research Report

The transcriptional regulation by E-Id protein axis upon T cell activation and its cellular metabolism

Research Project

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Project/Area Number 16H05205
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Immunology
Research InstitutionKyoto University

Principal Investigator

Miyazaki Masaki  京都大学, ウイルス・再生医科学研究所, 准教授 (80403632)

Research Collaborator Miyazaki Kazuko  
Project Period (FY) 2016-04-01 – 2019-03-31
KeywordsT細胞 / 分化・活性化 / 転写因子 / E2A, Id2, Id3
Outline of Final Research Achievements

We have worked on the study how the balance of E-protein and Id-protein regulates T cell development and activation for this three years. During this process, we discovered that E2A and HEB, members of E-protein, is essential for the T cell lineage commitment in the thymus. Simultaneously, E2A and HEB suppresses the Innate lymphoid cell (ILC) lineage in the thymus, such as ILC2 and LTi-like cells.Given that the similarity of T cell and ILCs was demonstrated, This mechanisms of how developmental bifurcation of T cell and ILCs are regulated is very important findings for the understanding of cell differentiation in biology.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

本研究課題から、細胞分化の分岐点において、転写因子群は非常に洗練された調節システムを持っており、そのバランスによって、様々な機能を持った細胞群へと分岐し、その機能を発揮する。このような細胞分化の多様性により、生物個体としての全体の機能を発揮することができる。今回は、獲得免疫と自然免疫を担当する、T細胞と自然リンパ球の分化の分岐点を解明し、生物の緻密な分化の一端を明らかにした。

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Published: 2020-03-30  

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