Identification of Renal Long Non-coding RNA RP11-2B6.2 as a Positive Regulator of Type I Interferon Signaling Pathway in Lupus Nephritis

Conclusion: The expression of lncRNAs is abnormal in the kidney of LN. LncRNA RP11-2B6.2 is a novel positive regulator of IFN-I pathway through epigenetic inhibition of SOCS1, which provides a new therapeutic target to alleviate over-activated IFN-I signaling in LN. Introduction Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disorder characterized by the occurrence of a wide range of autoantibodies and organ damage and predominantly affects women at childbearing age (1, 2). Lupus nephritis (LN) is considered one of the most prevalent and serious complications of SLE with high morbidity and mortality (3–5). Routine therapies for LN are largely based on steroids and non-specific immunosuppressants, most of which are prone to irreversible gastric-ulcer and life-threatening leucopenia (6). In-depth investigation of the molecular mechanisms for the dysregulation of immune responses will facilitate the discovery of new therapeutic targets with reduced adverse effects and improved curative efficacy. Long non-coding RNAs (lncRNAs) (>200 nucleotides in length) are a class of widespread transcriptional outputs (7, 8), and have been recognized as important regulators in many physiological or pathological processes. Our previous studies have indicated a link between the dysregulation of lncRNAs in peripheral blood mononuclear cells (PBMCs) and disease activity of SLE. For example, linc0949 is decreased in PBMCs of SLE patients and the expression...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research