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Pauline Santa1†
Anne Garreau1†
Lee Serpas2†
Amandine Ferriere1
Patrick Blanco1,3
Chetna Soni2*
Vanja Sisirak1*- 1CNRS-UMR 5164, ImmunoConcEpT, Bordeaux University, Bordeaux, France
- 2Department of Pathology, New York University Grossman School of Medicine, New York, NY, United States
- 3Immunology and Immunogenetic Department, Bordeaux University Hospital, Bordeaux, France
A Corrigendum on
The Role of Nucleases and Nucleic Acid Editing Enzymes in the Regulation of Self-Nucleic Acid Sensing
By Santa P, Garreau A, Serpas L, Ferriere A, Blanco P, Soni C and Sisirak V (2021). 12:629922. doi: 10.3389/fimmu.2021.629922
In the original article, there was a mistake in the legend for Figure 2 as published. The correct legend for Figure 2 was mistakenly omitted and replaced with the legend of figure 3. The correct legend appears below.
FIGURE 2
Figure 2 DNASE1L3 deficiency leads to systemic lupus erythematosus (SLE). DNASE1L3 deficiency leads to the accumulation of numerous forms of DNA including chromatin, MP associated DNA and NET-associated DNA. Accumulation of such DNA contributes to the aberrant activation of TLR7,9 in B cells and plasmacytoid dendritic cells (pDCs). In B cells TLR7,9 activation leads to their differentiation into plasma cells and antibody forming cells (AFC) that produce autoreactive antibodies mostly directed against dsDNA. In pDCs TLR7,9 activation induces the production of type I interferons (IFN-I) which also play an important role in the transition of B cells into AFC. The production of anti-dsDNA antibodies and of IFN-I will ultimately cause the development of Systemic Lupus Erythematosus (SLE).
DNASE1L3 deficiency leads to the accumulation of numerous forms of DNA including chromatin, MP associated DNA and NET-associated DNA. Accumulation of such DNA contributes to the aberrant activation of TLR7,9 in B cells and plasmacytoid dendritic cells (pDCs). In B cells TLR7,9 activation leads to their differentiation into plasma cells and antibody forming cells (AFC) that produce autoreactive antibodies mostly directed against dsDNA. In pDCs TLR7,9 activation induces the production of type I interferons (IFN-I) which also play an important role in the transition of B cells into AFC. The production of anti-dsDNA antibodies and of IFN-I will ultimately cause the development of Systemic Lupus Erythematosus (SLE).
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Keywords: DNases, RNases, systemic lupus erythematosus, DNA sensing, RNA sensing, interferonopathies, aicardi goutieres syndrome, toll-like receptors
Citation: Santa P, Garreau A, Serpas L, Ferriere A, Blanco P, Soni C and Sisirak V (2021) Corrigendum: The Role of Nucleases and Nucleic Acid Editing Enzymes in the Regulation of Self-Nucleic Acid Sensing. Front. Immunol. 12:690853. doi: 10.3389/fimmu.2021.690853
Received: 04 April 2021; Accepted: 08 April 2021;
Published: 22 April 2021.
Edited and reviewed by: Nadine Laguette, Centre National de la Recherche Scientifique (CNRS), France
Copyright © 2021 Santa, Garreau, Serpas, Ferriere, Blanco, Soni and Sisirak. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Chetna Soni, Y2hldG5hLnNvbmlAbnl1bGFuZ29uZS5vcmc=; Vanja Sisirak, dnNpc2lyYWtAaW1tdWNvbmNlcHQub3Jn
†These authors have contributed equally to this work