Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/121748
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Type: Journal article
Title: IFNL3 genotype is associated with pulmonary fibrosis in patients with systemic sclerosis
Author: Metwally, M.
Thabet, K.
Bayoumi, A.
Nikpour, M.
Stevens, W.
Sahhar, J.
Zochling, J.
Roddy, J.
Tymms, K.
Strickland, G.
Lester, S.
Rischmueller, M.
Ngian, G.-S.
Walker, J.
Hissaria, P.
Shaker, O.
Liddle, C.
Manolios, N.
Beretta, L.
Proudman, S.
et al.
Citation: Scientific Reports, 2019; 9(1):14834-14834
Publisher: Nature Publishing Group
Issue Date: 2019
ISSN: 2045-2322
2045-2322
Statement of
Responsibility: 
Mayada Metwally, Khaled Thabet ... Susan Lester, Maureen Rischmueller ... Pravin Hissaria ... Susanna Proudman ... et al.
Abstract: Fibrosis across different organs and tissues is likely to share common pathophysiological mechanisms and pathways. Recently, a polymorphism (rs12979860) near the interferon lambda gene (IFNL3) was shown to be associated with fibrosis in liver across multiple disease etiologies. We determined whether this variant is a risk factor for pulmonary fibrosis (PF) and worsening cutaneous fibrosis in systemic sclerosis (SSc). Caucasian patients with SSc (n = 733) were genotyped to test for association with the presence of PF and worsening of skin fibrosis. Serum IFN-λ3 levels from 200 SSc cases were evaluated. An association of the IFNL3 polymorphism with PF was demonstrated (OR: 1.66 (95% CI: 1.142-2.416, p = 0.008). The IFNL3 variant was not a risk factor for worsening of skin fibrosis. Functionally, IFN-λ3 serum levels were higher among subjects with PF compared to those unaffected (P < 0.0001). In conclusion, IFNL3 serum levels and the genetic variant known to be associated with liver fibrosis are similarly linked to PF, but not to worsening of skin fibrosis in SSc. These data highlight both common fibrosis pathways operating between organs, as well as differential effects within the same disease.
Keywords: Genetics research; translational research
Rights: © The Author(s) 2019. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
DOI: 10.1038/s41598-019-50709-9
Grant ID: http://purl.org/au-research/grants/nhmrc/1053206
http://purl.org/au-research/grants/nhmrc/1071735
http://purl.org/au-research/grants/nhmrc/1107178
http://purl.org/au-research/grants/nhmrc/1108422
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