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--- sle [2025/11/14 10:52] – [aetiology] gary1
+++ sle [2025/11/14 11:01] (current) – [aetiology] gary1
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   *potential pathophysiologic mechanisms:
     *a single genetic mutation in the UNC93B1 gene may be the trigger for a form of the autoimmune disease lupus in children(([[https://www.sciencealert.com/lupus-tracked-to-changes-in-a-single-gene-that-tames-the-immune-system]]))
-    *[[EBV]] infections in susceptible people perhaps by certain strains of EBV result in activation of pro-inflammatory genes in B cells which appear to mediate SLE(([[https://www.sciencealert.com/scientists-trace-lupus-to-one-of-the-worlds-most-common-viruses]]))
+    *[[EBV]] infections in susceptible people perhaps by certain strains of EBV produce a protein called EBNA2 which results in activation of pro-inflammatory genes (ZEB2 and TBX21) in B memory cells which appear to mediate SLE(([[https://www.sciencealert.com/scientists-trace-lupus-to-one-of-the-worlds-most-common-viruses]]))(([[https://www.newscientist.com/article/2504061-strongest-evidence-yet-that-the-epstein-barr-virus-causes-lupus/]]))
     * ETV5 (a specific transcription factor expressed in T cells) enhances the expression of its target protein, osteopontin (OPN) which in turn activates the AKT protein, leading to the differentiation into T follicular helper (TFH) cells potentially leading to SLE. An overabundance of TFHs can cause B cells to become overly active, resulting in autoimmune diseases. In such cases, B cells mistakenly recognize the body's own tissues and cells as pathogens and produce autoantibodies even when no external pathogens are present. (([[https://www.news-medical.net/news/20240701/Researchers-discover-role-of-particular-protein-in-the-development-of-lupus.aspx]]))