TY - JOUR
T1 - Serum proteomic profiling of rheumatoid arthritis–interstitial lung disease with a comparison to idiopathic pulmonary fibrosis
AU - Wu, Xiaoping
AU - Jeong, Yunju
AU - de Frías, Sergio Poli
AU - Easthausen, Imaani
AU - Hoffman, Katherine
AU - Oromendia, Clara
AU - Taheri, Shahrad
AU - Esposito, Anthony J.
AU - Arias, Luisa Quesada
AU - Ayaub, Ehab A.
AU - Maurer, Rie
AU - Gill, Ritu R.
AU - Hatabu, Hiroto
AU - Nishino, Mizuki
AU - Frits, Michelle L.
AU - Iannaccone, Christine K.
AU - Weinblatt, Michael E.
AU - Shadick, Nancy A.
AU - Dellaripa, Paul F.
AU - Choi, Augustine M.K.
AU - Kim, Edy Y.
AU - Rosas, Ivan O.
AU - Martinez, Fernando J.
AU - Doyle, Tracy J.
N1 - Funding Information:
We offer our sincere thanks to the patients with rheumatoid arthritis who participated and to the staff of BRASS and the Arthritis Center at Brigham and Women’s Hospital for their efforts in this study. This work was supported by the National Institutes of Health (grant numbers K23 HL119558 and R03 HL148484) and Stony Wold-Herbert Fund Fellowship Grant (no grant number applicable). The Brigham Rheumatoid Arthritis Sequential Study is funded by grants from Bristol-Myers Squibb, Amgen, Crescendo Bioscience and Sanofi/Regeneron. The authors would like to thank the Clinical Research and Proteomics Cores at Weill Cornell Medicine–Qatar, supported by the Biomedical Research Program funded by Qatar Foundation. The funders had no role in study design, data collection, analysis, decision to publish or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard University, Weill Cornell Medicine, their affiliated academic healthcare centers or the National Institutes of Health.
Funding Information:
This work was supported by the National Institutes of Health (grant numbers K23 HL119558 and R03 HL148484) and Stony Wold-Herbert Fund Fellowship Grant (no grant number applicable). The Brigham Rheumatoid Arthritis Sequential Study is funded by grants from Bristol-Myers Squibb, Amgen, Crescendo Bioscience and Sanofi/Regeneron. The authors would like to thank the Clinical Research and Proteomics Cores at Weill Cornell Medicine–Qatar, supported by the Biomedical Research Program funded by Qatar Foundation. The funders had no role in study design, data collection, analysis, decision to publish or preparation of the manuscript. The content is solely the responsibility of the authors and does not necessarily represent the official views of Harvard University, Weill Cornell Medicine, their affiliated academic healthcare centers or the National Institutes of Health.
Publisher Copyright:
© Author(s)
PY - 2022/7/30
Y1 - 2022/7/30
N2 - Although interstitial lung disease (ILD) causes significant morbidity and mortality in rheumatoid arthritis (RA), it is difficult to predict the development or progression of ILD, emphasising the need for improved discovery through minimally invasive diagnostic tests. Aptamer-based proteomic profiling was used to assess 1321 proteins from 159 patients with rheumatoid arthritis with interstitial lung disease (RA-ILD), RA without ILD, idiopathic pulmonary fibrosis and healthy controls. Differential expression and gene set enrichment analyses revealed molecular signatures that are strongly associated with the presence and severity of RA-ILD and provided insight into unexplored pathways of disease. These warrant further study as non-invasive diagnostic tools and future therapeutic targets.
AB - Although interstitial lung disease (ILD) causes significant morbidity and mortality in rheumatoid arthritis (RA), it is difficult to predict the development or progression of ILD, emphasising the need for improved discovery through minimally invasive diagnostic tests. Aptamer-based proteomic profiling was used to assess 1321 proteins from 159 patients with rheumatoid arthritis with interstitial lung disease (RA-ILD), RA without ILD, idiopathic pulmonary fibrosis and healthy controls. Differential expression and gene set enrichment analyses revealed molecular signatures that are strongly associated with the presence and severity of RA-ILD and provided insight into unexplored pathways of disease. These warrant further study as non-invasive diagnostic tools and future therapeutic targets.
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U2 - 10.1136/thorax-2021-217822
DO - 10.1136/thorax-2021-217822
M3 - Article
C2 - 35907639
AN - SCOPUS:85142021902
VL - 77
SP - 1041
EP - 1044
JO - Thorax
JF - Thorax
SN - 0040-6376
IS - 10
ER -