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

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293017
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Biological pharmacy
• Research Institution: Tokushima 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