LIG4 and RAD52 DNA repair genes polymorphisms and systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a complex autoimmune disorder with a strong genetic background. Nevertheless, SLE might also be triggered due to environmental factors, such as UV light exposure. DNA double strand breaks (DSBs) may be induced secondarily by UV radiation, increasing DNA immunogenicity and in SLE patients DNA repair is diminished, allowing the accumulation of DSBs and genomic instability.

Polymorphisms in STK17A gene are associated with systemic lupus erythematosus and its clinical manifestations.

Systemic lupus erythematosus (SLE) is an autoimmune disorder with several clinical manifestations. SLE etiology has a strong genetic component, which plays a key role in disease's predisposition, as well as participation of environmental factors, such and UV light exposure. In this regard, we investigated whether polymorphisms in STK17A, a DNA repair related gene, encoding for serine/threonine-protein kinase 17A, are associated with SLE susceptibility.

FYB gene polymorphisms are associated with susceptibility for systemic lupus erythemathosus (SLE).

Systemic Lupus Erythematosus (SLE) is a multifactorial autoimmune disease affecting different organs or systems. Several genes have been associated with SLE susceptibility so far. A previous study has reported, in SLE patients, a differential expression of Fyn Binding Protein gene (FYB), encoding for a protein participating in the T cells signaling cascade and in the interleukin-2A expression modulation.