|
ヤマグチ ルイ
Rui Yamaguchi
山口 類 所属 熊本保健科学大学 保健科学部 医学検査学科 熊本保健科学大学大学院 保健科学研究科 保健科学専攻 職位 准教授 |
|
| 発表年月日 | 2021/10/08 |
| 発表テーマ | Adaptive Immunity: The Role of Toll-Like Receptors |
| 会議名 | The organizing committee of the 6th AHSS 2021 Kumamoto Health Science University |
| 学会区分 | 国際学会 |
| 発表形式 | 口頭（一般） |
| 単独共同区分 | 単独 |
| 国名 | 日本 |
| 開催地名 | Kumamoto Health Science University |
| 開催期間 | 2021/10/08～2021/10/08 |
| 発表者・共同発表者 | Rui Yamaguchi ,Yasuo Yamaguchi |
| 概要 | Resiquimod significantly enhanced IL-23 expression by macrophages, whereas LPS enhanced it only slightly. Furthermore,sequential stimulation of human macrophages with LPS and
resiquimod significantly reduced IL-23 levels, as determined by ELISA. LPS upregulated TNFAIP3 expression by human macrophages, as also determined by ELISA. After exposure to resiquimod, small interfering RNA for TGFβ1/2/3 or TAK-1 decreased IL-23 levels. Adaptive immunity is triggered by activation of TLRs, which induce innate immunity. Activation of TLR4 promotes TNFAIP3 generation by human macrophages. TNFAIP3 has both ubiquitinase and deubiquitinase activity and regulates the TLR7/8 signaling pathway to enhance IL-23 production. IL-23 maintains Th17 cells and is involved in the development of autoimmune diseases through adaptive immune responses. Adaptive immunity is controlled by cross-talk between TLRs activated by the innate immune system. |