Authors: Leslie A. Nangle, Zhiwen Xu, David Siefker, Christoph Burkart, Yeeting E. Chong, Liting Zhai, Yanyan Geng, Clara Polizzi, Lauren Guy, Lisa Eide, Yao Tong, Sofia Klopp-Savino, Michaela Ferrer, Kaitlyn Rauch, Annie Wang, Kristina Hamel, Steve Crampton, Suzanne Paz, Kyle P. Chiang, Minh-Ha Do, Luke Burman, Darin Lee, Mingjie Zhang, Kathleen Ogilvie, David King, Ryan A. Adams, Paul Schimmel
Published: 2025-03-12
DOI: 10.1126/scitranslmed.adp4754
Source: Full article
Interstitial lung disease (ILD) consists of a group of immune-mediated disorders that can cause inflammation and progressive fibrosis of the lungs, representing an area of unmet medical need given the lack of disease-modifying therapies and toxicities associated with current treatment options. Tissue-specific splice variants (SVs) of human aminoacyl-tRNA synthetases (aaRSs) are catalytic nulls thought to confer regulatory functions. One example from human histidyl-tRNA synthetase (HARS), termed HARS