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Abstract
Deoxyribonucleases (DNases) might play a role in prevention of autoimmune conditions such as systemic lupus erythematosus through clearance of cell debris resulting from apoptosis and/or necrosis. Previous studies have suggested that variations in the in vivo activities of DNases I-like 3(1L3) and II have an impact on autoimmune-related conditions. The genes for these DNases are known to show copy number variations (CNVs) whereby copy loss leads to a reduction of the in vivo activities of the enzymes, thereby possibly affecting the pathophysiological background of autoimmune diseases. Using a simple newly developed quantitative real-time PCR method, we investigated the distributions of the CNVs for DNASE1L3 and DNASE2 in Japanese and German populations. It was found that only 2 diploid copy numbers for all of these DNASE CNVs was distributed in both of the study populations; no copy loss or gain was evident for any of the autoimmune-related DNase genes. Therefore, it was demonstrated that these human autoimmune-related DNase genes show low genetic diversity of CNVs resulting in alterations of the in vivo levels of DNase activity.
Highlights
It has been suggested that deoxyribonuclease (DNase)-mediated clearance of cell debris resulting from apoptosis and/or necrosis might be primarily involved in the prevention of autoimmune conditions such as systemic lupus erythematosus (SLE) [1,2]
In the context of autoimmunity, it has been postulated that DNase I-like 3 (DNase 1L3) in serum break down chromatin during apoptosis and/or necrosis [3,4], while DNase II in lysosomes is involved in the degradation of endogenous DNA in apoptotic cells that have been engulfed by macrophages [5,6]
Since the quantitative accuracy of quantitative real-time PCR (Q-PCR) analysis depends on proper normalization, these results demonstrated that copy number estimation using this method was reliable
Summary
It has been suggested that deoxyribonuclease (DNase)-mediated clearance of cell debris resulting from apoptosis and/or necrosis might be primarily involved in the prevention of autoimmune conditions such as systemic lupus erythematosus (SLE) [1,2]. In the context of autoimmunity, it has been postulated that DNase I-like 3 (DNase 1L3) in serum break down chromatin during apoptosis and/or necrosis [3,4], while DNase II in lysosomes is involved in the degradation of endogenous DNA in apoptotic cells that have been engulfed by macrophages [5,6].
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