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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 |
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| 言語種別 | 英語 |
| 発行・発表の年月 | 2021/07 |
| 形態種別 | 研究論文（学術雑誌） |
| 査読 | 査読あり |
| 標題 | Adaptive immunity: the role of toll-like receptors. |
| 執筆形態 | 共著 |
| 掲載誌名 | Austin J Allergy. 2 |
| 掲載区分 | 国外 |
| 巻・号・頁 | 7(1) |
| 担当区分 | 筆頭著者 |
| 著者・共著者 | Rui Yamaguchi, Arisa Sakamoto, Reona Yamaguchi, Misa Haraguchi,
Shinji Narahara, Hiroyuki Sugiuchi and Yasuo Yamaguchi |
| 概要 | The central mediators of the adaptive immune response are T cells. The clonal
expansion of T cells required for adaptive immunity results from the innate immune response, which is triggered by the stimulation of toll-like receptors (TLRs). The adaptive immune response can cause autoimmune diseases, and Th17 cells are known to contribute to several autoimmune diseases. Pathogenic Th17 cells are induced by interleukin 23 (IL-23) and IL-1β. Resiquimod (a TLR7/8 agonist) significantly enhances IL-23 production by human macrophages, and lipopolysaccharide (a TLR4 agonist) slightly enhances it. Interestingly, IL-23 levels are significantly attenuated after sequential stimulation with lipopolysaccharide and resiquimod, indicating cross-talk between the TLR4 and TLR7/8 signaling pathways. In this review, we discuss the pivotal role of TLRs in triggering innate immunity and inducing adaptive immunity, leading to autoimmune diseases. |