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.
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.