Reviews
Role of TLR7 in the pathogenesis of primary Sjögren's syndrome
Y. Song1, W. Zhou2
- Beijing Tiantan Hospital, Capital Medical University, Beijing, and Department of Oral Medicine, Beijing Stomatological Hospital, Capital Medical University, Beijing, China.
- Beijing Tiantan Hospital, Capital Medical University, Beijing, and Rheumatology and Immunology Department, Beijing Tiantan Hospital, Beijing, China. weizhou0925@126.com
CER17182
2024 Vol.42, N°12
PI 2513, PF 2519
Reviews
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PMID: 38489320 [PubMed]
Received: 30/09/2023
Accepted : 08/01/2024
In Press: 12/03/2024
Published: 19/12/2024
Abstract
Primary Sjögren’s syndrome (pSS) is an autoimmune disorder characterised by immune-driven damage to the exocrine glands, leading to diminished salivary and tear production. While the pathogenesis of pSS remains incompletely understood, its clinical presentations vary widely, and no specific treatments are currently available. Toll-like receptor 7 (TLR7) belongs to the Toll-like receptor family and is crucial for the innate immune response, notably in recognising pathogenic patterns. TLR7 is predominantly found in the endoplasmic reticulum (ER) and endosomes, where it identifies single-stranded RNA (ssRNA). Upon ligand binding, TLR7 activates the Myd88-dependent signalling cascade, eliciting an immune response. Dysregulation and variations in TLR7 expression are implicated in several autoimmune disorders. In genetically predisposed individuals, factors such as infections, endocrinological abnormality and metabolic abnormalities can cause TLR7 dysregulation, aggravating pSS symptoms and progression. While studies on TLR7 in pSS are limited, they offer insights into the disease’s pathophysiological processes, vital for the treatment and prognosis. This article explores the mechanisms of TLR7 dysregulation, its involvement in pSS pathogenesis, and prospective therapeutic significance.
