{"title":"Toll-like receptors 7 and 8 as therapeutic targets for human diseases.","authors":"Ryutaro Fukui, Kensuke Miyake","doi":"10.1093/intimm/dxag052","DOIUrl":null,"url":null,"abstract":"<p><p>Toll-like receptor 7 (TLR7) and TLR8 respond to pathogen-derived single-stranded RNA (ssRNA), orchestrating innate immune defense responses upon infections. However, aberrant recognition of endogenous ssRNAs by these sensors can cause various pathologies, including systemic lupus erythematosus (SLE), familial histiocytosis, immunodeficiency, and bone marrow failure. Recent insights into genetic variations in TLR7/8 and functionally associated genes have elucidated the mechanisms that prevent excessive TLR7/8 activation. Specifically, TLR7/8 responses are negatively regulated by several mechanisms, including the TLR-specific chaperone UNC93B1, lysosomal NADPH oxidase NOX2, the lysosomal nuclease PLD4, and the lysosomal nucleoside transporter SLC29A3. Given the link between dysregulated TLR7/8 activation and diseases development, therapeutic agents targeting these receptors are currently under clinical trials to evaluate their efficacy in treating SLE.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":" ","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/intimm/dxag052","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Toll-like receptor 7 (TLR7) and TLR8 respond to pathogen-derived single-stranded RNA (ssRNA), orchestrating innate immune defense responses upon infections. However, aberrant recognition of endogenous ssRNAs by these sensors can cause various pathologies, including systemic lupus erythematosus (SLE), familial histiocytosis, immunodeficiency, and bone marrow failure. Recent insights into genetic variations in TLR7/8 and functionally associated genes have elucidated the mechanisms that prevent excessive TLR7/8 activation. Specifically, TLR7/8 responses are negatively regulated by several mechanisms, including the TLR-specific chaperone UNC93B1, lysosomal NADPH oxidase NOX2, the lysosomal nuclease PLD4, and the lysosomal nucleoside transporter SLC29A3. Given the link between dysregulated TLR7/8 activation and diseases development, therapeutic agents targeting these receptors are currently under clinical trials to evaluate their efficacy in treating SLE.
期刊介绍：
International Immunology is an online only (from Jan 2018) journal that publishes basic research and clinical studies from all areas of immunology and includes research conducted in laboratories throughout the world.
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