| Literature DB >> 28089741 |
Birutė Tumienė1, Norine Voisin2, Eglė Preikšaitienė3, Donatas Petroška4, Jurgita Grikinienė5, Rūta Samaitienė5, Algirdas Utkus3, Alexandre Reymond2, Vaidutis Kučinskas3.
Abstract
Aicardi-Goutières syndrome (AGS) is an inflammatory disorder belonging to the recently characterized group of type I interferonopathies. The most consistently affected tissues in AGS are the central nervous system and skin, but various organ systems and tissues have been reported to be affected, pointing to the systemic nature of the disease. Here we describe a patient with AGS due to a homozygous p.Arg114His mutation in the TREX1 gene. The histologically proven inflammatory myopathy in our patient expands the range of clinical features of AGS. Histological signs of muscle biopsies in the proband, and in two other AGS patients described earlier, are similar to those seen in various autoimmune myositises and could be ascribed to inapproapriate IFN I activation. In view of signs of possible mitochondrial damage in AGS, we propose that mitochondrial DNA could be a trigger of autoimmune responses in AGS.Entities:
Keywords: Aicardi-Goutières syndrome; Autoimmune myositis; Exome sequencing; Inflammatory myopathy; Type I interferonopathy
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Year: 2017 PMID: 28089741 DOI: 10.1016/j.ejmg.2016.12.004
Source DB: PubMed Journal: Eur J Med Genet ISSN: 1769-7212 Impact factor: 2.708