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2014 Fiscal Year Final Research Report

Molecular mechanisms of Th9 cell-mediated chronic inflammation

Research Project

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Project/Area Number 25893033
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeSingle-year Grants
Research Field Immunology
Research InstitutionChiba University

Principal Investigator

YAGI Ryoji  千葉大学, 医学(系)研究科(研究院), 特任准教授 (20392152)

Project Period (FY) 2013-08-30 – 2015-03-31
Keywords免疫学 / アレルギー・ぜんそく / Th9 / ヘルパーT細胞 / 遺伝子発現制御 / サイトカイン / IL-9
Outline of Final Research Achievements

Naive CD4 T cells can differentiate into several T helper (Th) cell subsets, Th1, Th2, Th17, regulatory T cells and follicular T cells. Recently Th9 cells have been added into Th cell subsets. Th9 cells are known to induce proliferation of mast cells and secretion of mucus from goblet cells and also to be involved in allergic diseases. IL-4 and TGFβ are required for Th9 cell differentiation from naive CD4 T cells in vitro. However, the molecular mechanism of Th9 cell differentiation and the function of Th9 cells in vivo are not understood yet. To study these questions, we focused on a responsible gene which we found previously and we established an in vivo model to investigate role of the gene on Th9 cell differentiation.

Free Research Field

免疫学

URL: 

Published: 2016-06-03  

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