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The Ro60 autoantigen binds endogenous retroelements and regulates inflammatory gene expression
T Hung1, G A Pratt2, B Sundararaman2
1Genentech, South San Francisco, CA 94080, USA. behrens.tim@gene.com hungt2@gene.com geneyeo@ucsd.edu.
Science (New York, N.Y.)
|September 19, 2015
Summary
Autoantibodies targeting Ro60 in lupus are linked to Alu retroelements. These elements, when bound by Ro60, promote inflammation, suggesting a role in systemic lupus erythematosus pathogenesis.
Area of Science:
- Molecular biology
- Immunology
- Genetics
Background:
- Autoantibodies to Ro60 are common in systemic lupus erythematosus (SLE) and Sjögren's syndrome.
- The role of Ro60 and its associated RNAs in disease pathogenesis remains unclear.
Purpose of the Study:
- To investigate the association between Ro60 and its bound RNAs.
- To determine the contribution of Ro60-associated RNAs to type I interferon signaling and inflammation in SLE.
Main Methods:
- Cataloging Ro60-associated RNAs in human cell lines.
- Analyzing Alu retroelement transcript expression and induction by type I interferon.
- Assessing the impact of Ro60 deletion on Alu RNA and interferon-regulated gene expression.
- Detecting Alu RNAs in anti-Ro60-positive SLE immune complexes and whole blood samples.
Main Results:
- Ro60 binds to RNA motifs derived from endogenous Alu retroelements.
- Alu transcripts are induced by type I interferon and stimulate proinflammatory cytokine secretion.
- Ro60 deletion leads to increased Alu RNA and interferon-regulated gene expression.
- Alu RNAs are present in SLE immune complexes and upregulated in SLE blood samples.
Conclusions:
- Establishes a link between the lupus autoantigen Ro60, Alu retroelements, and type I interferon.
- Suggests that Alu retroelements and their interaction with Ro60 contribute to SLE pathogenesis.
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