Activation ınduced-cytidine deaminase (AID) gene transcription analysis of antiphospholipid syndrome

Antiphospholipid syndrome (APS), a disease characterized by the presence of arterial and venous thrombosis tendency, recurrent abortions and antiphospholipid antibodies. The development of thrombosis in APS; negatively charged phospholipids and phospholipid-protein complexes formed against with antiphospholipid antibodies (lupus anticoagulant, anticardiolipin antibodies and anti-ß2-glycoprotein I antibodies) are thought to be responsible in the clinical features. There are three main B-lymphocyte mechanism which caused Immunoglobulin (Ig) diversity. These are somatic hypermutation (SHM), Ig gene conversion (GC) and class switch recombination (CSR). These three important mechanisms have been shown to be controlled by an enzyme called AID (Activation Induced Cytidine Deaminase), and also it has been shown that AID can cause breaking the stability of the genome and creating DNA damages in non-Ig genes.In this study, by measuring expression levels of AID gene which leads to immune diversity, we aimed to identify its effect of autoimmunity on APS. 70 APS patient and 70 healthy individuals peripheral blood samples are used for total RNA isolation. cDNA has been prepared by using the total RNA isolated from the samples. Q-PCR has been evaluated by using the target gene (AID) and a reference gene (HPRT1) primers and probes and the reference and target cDNA?s have been replicated. The expression levels of the target gene and the references have been measured and the data have been analyzed statisticaly. The results of the statistical analyses have shown that the APS patients have 40 times increased expression levels on AID gene mRNA versus healty individuals.Increased expression levels of AID gene not only causes somatic hypermutation ratio but also has a probability to increas the production of autoantibodies. To sum up it has been seen that AID gene may has a key role on the production of autoantibodies in APS patients.