Genome-wide Association Study Identifies 27 Loci Influencing Concentrations of Circulating Cytokines and Growth Factors

Circulating cytokines and growth factors are regulators of inflammation and have been implicated in autoimmune and metabolic diseases. In this genome-wide association study (GWAS) of up to 8,293 Finns we identified 27 genome-widely significant loci (p < 1.2 × 10 ) for one or more cytokines. Fifte...

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Published in:American journal of human genetics Vol. 100; no. 1; p. 40
Main Authors: Ahola-Olli, Ari V, Würtz, Peter, Havulinna, Aki S, Aalto, Kristiina, Pitkänen, Niina, Lehtimäki, Terho, Kähönen, Mika, Lyytikäinen, Leo-Pekka, Raitoharju, Emma, Seppälä, Ilkka, Sarin, Antti-Pekka, Ripatti, Samuli, Palotie, Aarne, Perola, Markus, Viikari, Jorma S, Jalkanen, Sirpa, Maksimow, Mikael, Salomaa, Veikko, Salmi, Marko, Kettunen, Johannes, Raitakari, Olli T
Format: Journal Article
Language:English
Published: United States 05.01.2017
Subjects:
Autoimmune Diseases - genetics
Colitis, Ulcerative - genetics
Crohn Disease - genetics
Cytokines - blood
Female
Genome-Wide Association Study
Humans
Inflammation - genetics
Intercellular Signaling Peptides and Proteins - blood
Male
Multiple Sclerosis - genetics
Quantitative Trait Loci - genetics
ISSN:1537-6605, 1537-6605
Online Access:Get more information
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Summary:Circulating cytokines and growth factors are regulators of inflammation and have been implicated in autoimmune and metabolic diseases. In this genome-wide association study (GWAS) of up to 8,293 Finns we identified 27 genome-widely significant loci (p < 1.2 × 10 ) for one or more cytokines. Fifteen of the associated variants had expression quantitative trait loci in whole blood. We provide genetic instruments to clarify the causal roles of cytokine signaling and upstream inflammation in immune-related and other chronic diseases. We further link inflammatory markers with variants previously associated with autoimmune diseases such as Crohn disease, multiple sclerosis, and ulcerative colitis and hereby elucidate the molecular mechanisms underpinning these diseases and suggest potential drug targets.
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ISSN:1537-6605
1537-6605
DOI:10.1016/j.ajhg.2016.11.007