Asset Details
Do you wish to reserve the book?
Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus
Do you wish to request the book?
Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Human and Murine Toll-like Receptor-Driven Disease in Systemic Lupus Erythematosus
2024
Overview
The pathogenesis of systemic lupus erythematosus (SLE) is linked to the differential roles of toll-like receptors (TLRs), particularly TLR7, TLR8, and TLR9. TLR7 overexpression or gene duplication, as seen with the Y-linked autoimmune accelerator (Yaa) locus or TLR7 agonist imiquimod, correlates with increased SLE severity, and specific TLR7 polymorphisms and gain-of-function variants are associated with enhanced SLE susceptibility and severity. In addition, the X-chromosome location of TLR7 and its escape from X-chromosome inactivation provide a genetic basis for female predominance in SLE. The absence of TLR8 and TLR9 have been shown to exacerbate the detrimental effects of TLR7, leading to upregulated TLR7 activity and increased disease severity in mouse models of SLE. The regulatory functions of TLR8 and TLR9 have been proposed to involve competition for the endosomal trafficking chaperone UNC93B1. However, recent evidence implies more direct, regulatory functions of TLR9 on TLR7 activity. The association between age-associated B cells (ABCs) and autoantibody production positions these cells as potential targets for treatment in SLE, but the lack of specific markers necessitates further research for precise therapeutic intervention. Therapeutically, targeting TLRs is a promising strategy for SLE treatment, with drugs like hydroxychloroquine already in clinical use.
Publisher
MDPI AG
Subject
/ Animals
/ Antigens
/ B cells
/ Disease
/ Diseases
/ Genes
/ Genetic Predisposition to Disease
/ Humans
/ Kidneys
/ Kinases
/ Ligands
/ Lupus
/ Lupus Erythematosus, Systemic - genetics
/ Lupus Erythematosus, Systemic - metabolism
/ Melanoma
/ Mice
/ Proteins
/ Sensors
/ Systemic lupus erythematosus
/ Toll-Like Receptor 7 - genetics
/ Toll-Like Receptor 7 - metabolism
/ Toll-Like Receptor 8 - genetics
/ Toll-Like Receptor 8 - metabolism
