Analysis of Fas gene as the causative molecule of systemic lupus erythematosus in patients with IgA vasculitis (Henoch-Schönlein purpura)
DOI:
https://doi.org/10.35366/113829Keywords:
IgA vasculitis,, systemic lupus erythematosus, Fas, apoptosis, lymphoproliferative syndromeAbstract
IgA vasculitis (HSP) and systemic lupus erythematosus (SLE) are both immune diseases that could be more interrelated than currently thought. HSP is an immune disease characterized by systemic small vessel vasculitis and mesangial deposits of immunoglobulin A, which ultimately leads to failure in apoptotic clearance and to the generation of a chronic lymphoproliferative syndrome. SLE is an immune disease characterized by chronic systemic inflammation that affects multiple tissues and systems, and its origin lies in the formation of double-stranded anti-DNA antibodies, which in turn are generated by failures in apoptotic clearance. HSP can be considered as a triggering factor for the development of systemic lupus erythematosus probably as the result of alterations in the apoptotic clearance that we think could be related to the inhibition of non-coding long-chain RNA genes (ENST00000378432, ENST00000571370, uc001kfc.1 y uc010qna.2) in patients with HSP, that in consequence alters Fas gene (CD95) track and the functions of the tumor necrosis factor family, that in turn inhibits the secretion of phosphatidylserine which ultimately generates a lymphoproliferative syndrome which possibly activates the double-stranded anti-DNA antibodies, the origin of SLE.
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