Basic information of IFNAR1 :

Official Symbol of Gene	IFNAR1
Species	Homo sapiens
Entrez Gene ID	3454
Official Full Name	interferon alpha and beta receptor subunit 1
Also known as	AVP; IFRC; IFNAR; IFNBR; IMD106; IFN-alpha-REC
Gene Type	protein coding
dbXrefs	Ensembl:ENSG00000142166 MIM:107450; AllianceGenome:HGNC:5432
Map Location	21q22.11

Sample information of multiple sclerosis:

Detected Sample	CSF
Sample Detail	N/A
Detected Method	ELISA
Disease	MS
Disease subtype	RRMS
Population	N/A
Sample Size	One hundred twenty-six RRMS patients, six CIS patients, 21 control subjects with no evidence of the inflammatory disease, and 74 HCs were enrolled in the study upon signing an institutional review board–approved form

Literature information of multiple sclerosis :

Pubmed ID	24850724
Year	2014
Title	The Role of Endogenous IFN-b in the Regulation of Th17 Responses in Patients with Relapsing-Remitting Multiple Sclerosis

Results of multiple sclerosis :

Expression	up-regulation
Risk type	Disease risk
Result	In vivo recombinant IFN-b–1a treatment induced IFNAR1 and its downstream signaling molecules’ gene expression, suggesting that treatment reconstitutes a deficient endogenous IFN-b regulation of the CD4+ T cells’ pathogenic cytokine production in patients with MS.
Mechanism/Pathway	We identified that the endogenous IFN-b from serum of RRMS patients induced a significantly lower IFN-inducible gene expression in comparison with healthy controls. In addition, in vitro studies have revealed deficient endogenous and exogenous IFN-b signaling in the CD4+ cells derived from patients with MS. Interestingly, upon inhibition of the endogenous IFN-b signaling by silencing IFN regulatory factor (IRF) 7 gene expression, the resting CD4+ T cells secreted significantly higher level of IL-17A, IL-17F, IL-21, IL-22, and IL-9, suggesting that endogenous IFN-b suppresses the secretion of these pathogenic cytokines.