Autoimmunity risk- and protection-associated IL7RA genetic variants differentially affect soluble and membrane IL-7Rα expression.


Journal

Journal of autoimmunity
ISSN: 1095-9157
Titre abrégé: J Autoimmun
Pays: England
ID NLM: 8812164

Informations de publication

Date de publication:
02 2019
Historique:
received: 10 10 2018
accepted: 11 10 2018
pubmed: 22 10 2018
medline: 27 5 2020
entrez: 22 10 2018
Statut: ppublish

Résumé

Interleukin-7 receptor α-chain (IL7RA) haplotypes are associated with susceptibility to autoimmune diseases including type 1 diabetes (T1D). Previous studies found lower soluble IL-7Rα (sIL-7Rα) serum levels of the protection-associated IL7RA haplotype assumed to reduce IL-7 availability for self-reactive T cells. Also, a risk-associated IL7RA haplotype is accompanied by lower sIL-7Rα serum concentrations but no underlying mechanisms have been described and the causative polymorphism remains unknown. Here, we characterized functional implications of the nonsynonymous rs1494558 (Thr66Ile), which tags the protection-associated IL7RA haplotype, in HEK293T cells and serum samples of T1D patients with different haplotype carriers. Influence of risk- and protection-associated haplotypes on IL-7Rα was analyzed. The risk-associated Ile66 variant affected gel mobility and impaired secretion of the sIL-7Rα as well as expression of the membrane-associated (m)IL-7Rα in HEK293T cells. Serum sIL-7Rα analyses confirmed differential gel mobility of the Ile66 variant and found decreased sIL-7Rα serum levels of T1D patients carrying the Ile66-tagged haplotype. Differences in glycosylation were not causative for differential mobility but enhanced the effects on impaired secretion. Comparison of protection- and risk-associated haplotypes in a cell line-based in vitro model identified dominant effects of the protective haplotype tagged by rs6897932 (Ile244) on mIL-7Rα expression, whereas the risk haplotype mainly affected the sIL-7Rα. This study identified novel functional effects of the Ile66 IL7RA variant and characterized features of autoimmunity risk- and protection-associated haplotypes. The findings add to our understanding of how these haplotypes regulate sIL-7Rα and mIL-7Rα expression in T cells causing differential susceptibility to autoimmune diseases.

Identifiants

pubmed: 30342817
pii: S0896-8411(18)30588-2
doi: 10.1016/j.jaut.2018.10.003
pii:
doi:

Substances chimiques

Receptors, Interleukin-7 0
interleukin-7 receptor, alpha chain 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

40-47

Informations de copyright

Copyright © 2018 Elsevier Ltd. All rights reserved.

Auteurs

Christian Lundtoft (C)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany.

Julia Seyfarth (J)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany; German Center for Diabetes Research (DZD), 85764, Munich-Neuherberg, Germany.

Sonja Oberstrass (S)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany.

Joachim Rosenbauer (J)

German Center for Diabetes Research (DZD), 85764, Munich-Neuherberg, Germany; Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Center at Heinrich-Heine University Düsseldorf, 40225, Düsseldorf, Germany.

Christina Baechle (C)

German Center for Diabetes Research (DZD), 85764, Munich-Neuherberg, Germany; Institute for Biometrics and Epidemiology, German Diabetes Center, Leibniz Center at Heinrich-Heine University Düsseldorf, 40225, Düsseldorf, Germany.

Michael Roden (M)

Division of Endocrinology and Diabetology, Medical Faculty, Heinrich Heine University Düsseldorf, 40225, Düsseldorf, Germany; Institute for Clinical Diabetology, German Diabetes Center, Leibniz Center at Heinrich-Heine University Düsseldorf, 40225, Düsseldorf, Germany.

Reinhard W Holl (RW)

German Center for Diabetes Research (DZD), 85764, Munich-Neuherberg, Germany; Institute of Epidemiology and Medical Biometry, ZIBMT, University of Ulm, 89081, Ulm, Germany.

Ertan Mayatepek (E)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany.

Sebastian Kummer (S)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany.

Thomas Meissner (T)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany; German Center for Diabetes Research (DZD), 85764, Munich-Neuherberg, Germany.

Marc Jacobsen (M)

Department of General Pediatrics, Neonatology and Pediatric Cardiology, University Children's Hospital, Medical Faculty, 40225, Duesseldorf, Germany. Electronic address: marc.jacobsen@med.uni-duesseldorf.de.

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Classifications MeSH