Genetic basis of Type I Interferon excessive production in Neuropsychiatric Systemic Lupus Erythematosus

Neuropsychiatric systemic lupus erythematosus(NPSLE) is a severe complication of SLE that is defined for itsneurological and psychiatric symptoms. This autoimmune disorder includes both central nervous system(CNS)and peripheral nervous system(PNS) manifestation that can pathogenically be divided into inflammatory NPSLEand thrombotic/ischemic NPSLE. First pathogenic process can be characterized by neural dysfunction due tomicroglia dependent synapse loss that is originated from excessive type I interferon expression as a conclusion ofautoantibodies production against self-nuclear components. This pathway has triggered several genetic studies inorder to manage NPSLE by promising therapeutic strategies. Furthermore, several candidate genes for SLE andNPSLE susceptibility have been studied such as TREX1, TYK2 and many of them need to be more studied byconsidering autoantibodies and IFN producing pathways. Also there are different methods for curing this disease;Some of them are now accessible and some will be accessible in future by accurate understanding of NPSLEpathogenesis. Here we tried to gather suspicious genes in inflammatory NPSLE contributed pathways in order togive a way to future studies and therapeutic targets.

Keywords:

NPSLE , Interferon type 1 , Genetics , Autoantibody , Neuro inflammation