Literature DB >> 28623091

DNA repair and systemic lupus erythematosus.

Rithy Meas1, Matthew J Burak1, Joann B Sweasy2.   

Abstract

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with no known cure that affects at least five million people worldwide. Monozygotic twin concordance and familial aggregation studies strongly suggest that lupus results from genetic predisposition along with environmental exposures including UV light. The majority of the common risk alleles associated with genetic predisposition to SLE map to genes associated with the immune system. However, evidence is emerging that implicates a role for aberrant DNA repair in the development of lupus. Here we summarize our current knowledge of the potential association of lupus with mutations in DNA repair genes. We also discuss how defective or aberrant DNA repair could lead to the development of lupus.
Copyright © 2017. Published by Elsevier B.V.

Entities:  

Keywords:  Class switch recombination; Cytoplasmic DNA; DNA repair; Neoantigen; Somatic hypermutation; Systemic lupus erythematosus

Mesh:

Substances:

Year:  2017        PMID: 28623091      PMCID: PMC5543809          DOI: 10.1016/j.dnarep.2017.06.020

Source DB:  PubMed          Journal:  DNA Repair (Amst)        ISSN: 1568-7856


  114 in total

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7.  DNA glycosylase deficiency leads to decreased severity of lupus in the Polb-Y265C mouse model.

Authors:  Sesha L Paluri; Matthew Burak; Alireza G Senejani; Madison Levinson; Tania Rahim; Kaylyn Clairmont; Michael Kashgarian; Isabel Alvarado-Cruz; Rithy Meas; Marina Cardó-Vila; Caroline Zeiss; Stephen Maher; Alfred L M Bothwell; Erdem Coskun; Melis Kant; Pawel Jaruga; Miral Dizdaroglu; R Stephen Lloyd; Joann B Sweasy
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  8 in total

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