Reply to “Type I <scp>IFN</scp> Signature in <scp>NOTCH1</scp>‐Related Leukoencephalopathy”-Reference-Cited by-同舟云学术

Reply to “Type I IFN Signature in NOTCH1‐Related Leukoencephalopathy”

Published:2023-03-20 Issue:5 Volume:93 Page:1043-1045
ISSN:0364-5134
Container-title:Annals of Neurology
language:en
Short-container-title:Annals of Neurology

Author:

Verhoeven Dorit¹²,Tromp Samantha A. M.¹²,van der Knaap Marjo S.³⁴⁵^ORCID,Kuijpers Taco W.¹²

Affiliation:

1. Department of Pediatric Immunology, Rheumatology and Infectious Disease, Emma Children's Hospital Amsterdam University Medical Centers, Academic Medical Center, University of Amsterdam Amsterdam The Netherlands

2. Department of Experimental Immunology Amsterdam Institute for Infection and Immunity, Amsterdam University Medical Centers, University of Amsterdam Amsterdam The Netherlands

3. Department of Child Neurology, Emma Children's Hospital Amsterdam University Medical Centers, VU University Amsterdam and Amsterdam Neuroscience Amsterdam The Netherlands

4. Amsterdam Leukodystrophy Center, Emma Children's Hospital Amsterdam University Medical Centers Amsterdam The Netherlands

5. Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research VU University Amsterdam The Netherlands

Publisher

Wiley

Subject

Neurology (clinical),Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ana.26629

Reference5 articles.

1. Type I Interferon Signature in NOTCH1‐Related Leukoencephalopathy

2. Heterozygous NOTCH1 Variants Cause CNS Immune Activation and Microangiopathy

3. Methods for type I interferon detection and their relevance for clinical utility and improved understanding of rheumatic diseases;Lamot L;Clin Exp Rheumatol,2019

4. The interferon type I signature is present in systemic sclerosis before overt fibrosis and might contribute to its pathogenesis through high BAFF gene expression and high collagen synthesis

5. Serum IFNα2 levels are associated with disease activity and outperform IFN-I gene signature in a longitudinal childhood-onset SLE cohort

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