2008
DOI: 10.1016/j.cytogfr.2008.04.009
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Rheumatoid polyarthritis caused by a defect in DNA degradation

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Cited by 15 publications
(10 citation statements)
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References 79 publications
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“…40,63 These findings are consistent with earlier studies showing that injection of bacterial or mitochondrial DNA into joints induced arthritis mediated by macrophage-produced TNF, 64,65 and that a polymorphism in the 5’-regulatory region of the gene encoding DNase II confers increased risk for RA. 66 …”
Section: Autoimmune Diseasessupporting
confidence: 90%
See 1 more Smart Citation
“…40,63 These findings are consistent with earlier studies showing that injection of bacterial or mitochondrial DNA into joints induced arthritis mediated by macrophage-produced TNF, 64,65 and that a polymorphism in the 5’-regulatory region of the gene encoding DNase II confers increased risk for RA. 66 …”
Section: Autoimmune Diseasessupporting
confidence: 90%
“…37 Inflammatory responses might also be triggered by DNA that has been incompletely digested either extracellularly by DNase I or intracellularly by DNase II, as inferred by the existence of a few SLE patients with function-impairing DNase I mutations, 38 lupus development in mice deficient in DNase I, 39 and anemia or arthritis in mice deficient in DNase II. 40 Moreover, the 3’ repair exonuclease Trexl is mutated in patients with autoimmune Aicardi–Goutieres syndrome and chilblain lupus, which exhibit some clinical and biochemical overlaps with SLE. Trexl is known to metabolize reverse-transcribed RNA and to negatively regulate I FN-stimulatory DNA responses.…”
Section: Autoimmune Diseasesmentioning
confidence: 99%
“…Nonetheless, incompletely digested DNA can provoke inflammatory responses, as inferred by a few patients with SLE with mutations in DNase I (Yasutomo and others 2001), lupus-like manifestations in mice deficient in DNase I (Napirei and others 2000), and anemia or arthritis in mice deficient in DNase II (Nagata 2008). DNase I is the major serum endonuclease that degrades extracellular dsDNA, whereas DNase II is localized in lysosomes and degrades chromosomal DNA from apoptotic cells and nuclei expelled from erythroid precursors.…”
Section: Cytosolic Innate Sensors and Autoimmunitymentioning
confidence: 99%
“…Specifically with regard to nucleic acid-sensing TLRs, these pathways involve autoantibodies bound to subcellular particles containing self-nucleic acids, which are taken up by pDCs via FcR, or by B cells via BCRs specific for either antigenic determinants in the complex or the Fc portion of the autoantibodies ( The synergistic engagement of BCR and TLR induces enhanced B cell proliferation, whereas production of type I IFN by pDCs leads to B cell differentiation and immunoglobulin isotype switching. Free nucleic acids or particles containing such molecules (ie, nucleosomes, RNPs) can also interact with specific BCRs (Viglianti and others 2003), and recent evidence suggests that BCR signaling induces fusion of TLR9-containing endosomes with the internalized BCR into autophagosomes, thereby facilitating B cell activation (Chaturvedi and others 2008;Monroe and Keir 2008).…”
Section: Endosomal Tlrs and Systemic Autoimmunitymentioning
confidence: 99%
“…However, our data do not show a complementary up-regulation of TLRs, nor do they confirm that the up-regulation of MyD88 was caused by TLRs. It is interesting that Nagata reported up-regulation of IFN-inducible genes in DNase II-deficient mice, which develop a chronic polyarthritis resembling human RA, and they further found no involvement of a TLR system in the IFNβ gene activation in DNase II -/- embryos [26]. Kawane et al also recently showed that when BM cells from the DNase II-deficient mice were transferred to the wild-type mice, they developed arthritis [27].…”
Section: Discussionmentioning
confidence: 99%