Traffic on the TLR expressway-Reference-Cited by-同舟云学术

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Traffic on the TLR expressway

Published:2024-06-13 Issue:8 Volume:221 Page:
ISSN:0022-1007
Container-title:Journal of Experimental Medicine
language:en
Short-container-title:

Author:

Taft Justin¹^ORCID,Bogunovic Dusan¹^ORCID

Affiliation:

1. Columbia University Medical Center 1 Department of Pediatrics and Center for Genetic Errors of Immunity, , New York, NY, USA

Abstract

Genetic variation in UNC93B1, a key component in TLR trafficking, can lead to autoinflammation caused by increased TLR activity. Analysis of seven patient variants combined with a comprehensive alanine screen revealed that different regions of UNC93B1 selectively regulate different TLRs (Rael et al. https://doi.org/10.1084/jem.20232005; David et al. https://doi.org/10.1084/jem.20232066).

Publisher

Rockefeller University Press

Link

https://rupress.org/jem/article-pdf/doi/10.1084/jem.20240841/1929282/jem_20240841.pdf

Reference8 articles.

1. The interaction between the ER membrane protein UNC93B and TLR3, 7, and 9 is crucial for TLR signaling

2. Gain-of-function human UNC93B1 variants cause systemic lupus erythematosus and chilblain lupus

3. Unc93B1 Restricts Systemic Lethal Inflammation by Orchestrating Toll-like Receptor 7 and 9 Trafficking

4. Unc93B1 biases Toll-like receptor responses to nucleic acid in dendritic cells toward DNA- but against RNA-sensing

5. UNC93B1 mediates differential trafficking of endosomal TLRs

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