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2016 Fiscal Year Final Research Report

Cross-talk between Th cells and inflammatory macrophages in chronic inflammatory respiratory diseases

Research Project

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Project/Area Number 26461178
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Respiratory organ internal medicine
Research InstitutionUniversity of Tsukuba

Principal Investigator

MORISHIMA YUKO  筑波大学, 医学医療系, 准教授 (10375511)

Project Period (FY) 2014-04-01 – 2017-03-31
KeywordsTh1 / Th17 / T-bet / RORγt / 肺胞蛋白症 / 非結核性抗酸菌
Outline of Final Research Achievements

Overexpression of T-bet, a master transcription factor in Th1 cells, induced pulmonary alveolar proteinosis (PAP)-like disease in T-bet-transgenic mice (T-bet-tg). T-bet-tg alveoli with PAP phenotype showed remarkable reorganization of alveolar mononuclear phagocyte subpopulations and impaired function, in addition to augmented T-cell infiltration. PAP development in T-bet-tg was also found to be associated with increased migration of myeloid cells from the bone marrow into the peripheral blood.
We next investigated the role of Th1/Th17 balance in host responses against Mycobacterium avium complex (MAC) infection. Neutrophilic pulmonary inflammation following MAC infection was enhanced in T-bet-deficient mice and in mice overexpressing RORγt, a master regulator for Th17 cell development.
Our results suggest that imbalance of Th lineage-specific master regulatory transcription factors may be critical determinants for the development of PAP and host resistance to MAC infection.

Free Research Field

炎症性呼吸器疾患

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Published: 2018-03-22  

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