Coordination of retrotransposons and type I interferon with distinct interferon pathways in dermatomyositis, systemic lupus erythematosus and autoimmune blistering disease.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
30 11 2021
Historique:
received: 20 04 2021
accepted: 18 11 2021
entrez: 1 12 2021
pubmed: 2 12 2021
medline: 27 1 2022
Statut: epublish

Résumé

Type I interferon (IFN) plays a crucial role in innate and adaptive immunity, and aberrant IFN responses are involved in systemic autoimmune diseases, such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Type I IFNs can be induced by transcribed retrotransposons. The regulation of retrotransposons and type I IFN and the downstream IFN pathways in SLE, DM, and autoimmune blistering disease (AIBD) were investigated. The gene expression levels of retrotransposons, including LINE-1, type I-III IFNs, and IFN-stimulated genes (ISGs) in peripheral blood cells from patients with DM (n = 24), SLE (n = 19), AIBD (n = 14) and healthy controls (HCs, n = 10) were assessed by quantitative polymerase chain reaction. Upregulation of retrotransposons and IFNs was detected in DM patient samples, as is characteristic, compared to HCs; however, ISGs were not uniformly upregulated. In contrast, retrotransposons and IFNs, except for type II IFN, such as IFN-γ, were not upregulated in SLE. In AIBD, only some retrotransposons and type I interferons were upregulated. The DM, SLE, and AIBD samples showed coordinated expression of retrotransposons and type I IFNs and distinct spectra of IFN signaling. A positive correlation between LINE-1 and IFN-β1 was also detected in human cell lines. These factors may participate in the development of these autoimmune diseases.

Identifiants

pubmed: 34848794
doi: 10.1038/s41598-021-02522-6
pii: 10.1038/s41598-021-02522-6
pmc: PMC8632942
doi:

Substances chimiques

Interferon Type I 0
RNA, Messenger 0
Retroelements 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

23146

Informations de copyright

© 2021. The Author(s).

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Auteurs

Yuko Kuriyama (Y)

Department of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Akira Shimizu (A)

Department of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan. ashimizu@kanazawa-med.ac.jp.
Department of Dermatology, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Kahoku-gun, Ishikawa, 920-0293, Japan. ashimizu@kanazawa-med.ac.jp.

Saki Kanai (S)

Department of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Daisuke Oikawa (D)

Department of Pathobiochemistry, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Sei-Ichiro Motegi (SI)

Department of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

Fuminori Tokunaga (F)

Department of Pathobiochemistry, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Osamu Ishikawa (O)

Department of Dermatology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.

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