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Cell Rep. 2018 Apr 3;23(1):50-57. doi: 10.1016/j.celrep.2018.03.036.

Increased RNA Editing May Provide a Source for Autoantigens in Systemic Lupus Erythematosus.

Author information

1
The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 5290002, Israel.
2
Department of Mathematics, Bar-Ilan University, Ramat Gan 5290002, Israel; The Gonda Multidisciplinary Brain Research Center, Bar-Ilan University, Ramat Gan 5290002, Israel.
3
Cancer Research Center and the Wohl Institute for Translational Medicine, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel.
4
Laboratory of Tumor Immunology and Immunotherapy, The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 5290002, Israel.

Abstract

RNA-editing mechanisms, which induce nucleotide substitution in the RNA, increase transcript and protein diversities. Editing dysregulation has been shown to lead to grave outcomes, and transcriptome-wide aberrant RNA editing has been found in tumors. However, little is known about the involvement of editing in other diseases. Systemic lupus erythematosus (SLE) is a multisystemic autoimmune disease characterized by a loss of tolerance for autoantigens from various tissues and the production of multiple autoantibodies. Here, we show that blood samples from individuals with SLE have abnormally high levels of RNA editing, some of which affect proteins and potentially generate novel autoantigens. We suggest that elevated RNA editing, either by ADARs or APOBECs, may be involved in the pathophysiology of SLE, as well as in other autoimmune diseases, by generating or increasing the autoantigen load, a key requisite for the progression of autoimmunity.

KEYWORDS:

A-to-I editing; ADAR; APOBEC3; C-to-U editing; RNA editing; SLE; autoimmune disease; immune tolerance; neo-autoantigens; systemic lupus erythematosus

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