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Rui Yamaguchi
Department Kumamoto Health Science University Department of Medical Technology, Faculty of Health Science Kumamoto Health Science University Graduate School Division of Health Sciences, Graduate School of Health Sciences Position Associate Professor |
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| Date | 2021/10/08 |
| Presentation Theme | Adaptive Immunity: The Role of Toll-Like Receptors |
| Conference | The organizing committee of the 6th AHSS 2021 Kumamoto Health Science University |
| Conference Type | International |
| Presentation Type | Speech (General) |
| Contribution Type | Individual |
| Country | Japan |
| Venue | Kumamoto Health Science University |
| Holding period | 2021/10/08～2021/10/08 |
| Publisher and common publisher | Rui Yamaguchi ,Yasuo Yamaguchi |
| Details | 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. |