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Misa Haraguchi
Department Kumamoto Health Science University Department of Medical Technology, Faculty of Health Science Position Assistant Professor |
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| Language | English |
| Publication Date | 2021/07 |
| Type | |
| Peer Review | Peer reviewed |
| Title | Adaptive Immunity: The Role of Toll-Like Receptors |
| Contribution Type | |
| Journal | Austin Journal of Allergy |
| Journal Type | Another Country |
| Volume, Issue, Page | 7(1) |
| Author and coauthor | Rui Yamaguchi, Arisa Sakamoto, Reona Yamaguchi, Misa Haraguchi,
Shinji Narahara, Hiroyuki Sugiuchi and Yasuo Yamaguchi |
| Details | 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. |