Toll-like receptors 7 and 8 as therapeutic targets for human diseases

Clicks: 20
ID: 330855
2026
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Emerging

Ranked #33 of 48 articles by views in international immunology

Most read Least read

Bar heights use a square-root scale.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
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.
Reference Key
openalex_W7218443750 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Ryutaro Fukui, Kensuke Miyake
Journal international immunology
Year 2026
DOI
10.1093/intimm/dxag052
URL
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

No comments yet. Be the first to comment on this article.