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2016 Fiscal Year Final Research Report

The role of novel inflammatory helper T cells that are highly capable of producing IL-13 in allergic inflammatory diseases

Research Project

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Project/Area Number 26293017
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Biological pharmacy
Research InstitutionTokushima Bunri University

Principal Investigator

Iwata Makoto  徳島文理大学, 薬学部, 教授 (50160122)

Co-Investigator(Kenkyū-buntansha) 宋 時栄  徳島文理大学, 大学共同利用機関等の部局等, 教授 (00399693)
門脇 則光  香川大学, 医学部, 教授 (60324620)
Co-Investigator(Renkei-kenkyūsha) OHOKA Yoshiharu  徳島文理大学, 香川薬学部, 准教授 (60303971)
TAKEUCHI Hajime  徳島文理大学, 香川薬学部, 准教授 (00421298)
NAKATSUMA Aya (YOKOTA Aya)  徳島文理大学, 香川薬学部, 助教 (30446075)
Project Period (FY) 2014-04-01 – 2017-03-31
Keywordsアレルギー / 炎症 / レチノイン酸 / IL-13 / ヘルパーT細胞
Outline of Final Research Achievements

In vitamin A-deficient mice, oral tolerance was not normally induced. Furthermore, very strong IgG1 and IgE antibody responses could be induced against oral antigens in an IL-13-dependet manner. On the other hand, the CD103(-)CD11b(+) subset of mesenteric lymph node dendritic cells in these mice induced differentiation of novel inflammatory helper T cells that are highly capable of producing IL-13 and TNF-α in an IL-6-dependent manner. These T cells are suggested to participate in the IL-13-dependent antibody responses to oral antigens, and preferentially migrated into inflamed skin. Retinoic acid receptor-mediated signaling suppressed the induction of these helper T cells. TGF-β also suppressed their induction, but reciprocally enhanced the induction of IL-17A-producing T cells.

Free Research Field

医歯薬学

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Published: 2018-03-22  

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