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The Long Non-coding RNA NRIR Drives IFN-Response in Monocytes: Implication for Systemic Sclerosis
Barbara Mariotti1, Nila Hendrika Servaas2,3, Marzia Rossato2,3,4
1General Pathology Section, Department of Medicine, University of Verona, Verona, Italy.
Frontiers in Immunology
|February 27, 2019
Summary
This study identifies Negative Regulator of the Interferon (IFN) Response (NRIR) long non-coding RNA as upregulated in systemic sclerosis (SSc) patients. NRIR dysregulation contributes to the type I IFN signature in SSc, impacting disease pathogenesis.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Toll-like receptor 4 (TLR4) activation triggers signaling cascades producing type I interferons (IFNs) and IFN-stimulated genes (ISGs).
- Dysregulation of the Interferon (IFN) Response, involving IFN-induced long non-coding RNAs (lncRNAs), is implicated in autoimmune disorders.
- Systemic sclerosis (SSc) pathogenesis involves TLR activation and ISG upregulation, but the role of specific lncRNAs in its type I IFN signature is unclear.
Purpose of the Study:
- To identify lncRNAs modulated by TLR4 activation and associated with the type I IFN response in human monocytes.
- To investigate the role of these lncRNAs, particularly Negative Regulator of the IFN Response (NRIR), in the pathogenesis of systemic sclerosis (SSc).
- To explore the functional impact of NRIR on IFN-stimulated genes (ISGs) and its contribution to the type I IFN signature in SSc.
Main Methods:
- RNA sequencing was used to identify lncRNAs modulated by TLR4 activation (LPS) in human monocytes.
- Weighted Gene Co-expression Network Analysis (WGCNA) was employed to identify NRIR-specific gene modules.
- Experimental validation of NRIR's function involved NRIR-silencing in monocytes and analysis of target gene expression (e.g., CXCL10, CXCL11).
Main Results:
- A group of lncRNAs related to IFN and antiviral responses were identified and found upregulated in SSc patients' monocytes.
- Negative Regulator of the IFN Response (NRIR) was significantly upregulated in SSc monocytes, correlating with the IFN score.
- NRIR knockdown reduced the induction of IFN-related chemokines CXCL10 and CXCL11 in monocytes.
Conclusions:
- NRIR is a key lncRNA upregulated in systemic sclerosis (SSc) and associated with the type I IFN signature.
- NRIR influences the expression of IFN-stimulated genes (ISGs), including chemokines like CXCL10 and CXCL11.
- Dysregulation of NRIR in monocytes may contribute to the type I IFN signature observed in SSc patients.
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