These findings suggest that CD8+iTregs attenuate LPS-induced glomerular endothelial cell injury through blocking the activation of p38 MAPK and NF-κB in lupus-MGECs.
On the other hand, certain miRNAs, RFX1, defective ERK pathway signaling, Gadd45α and DNA hydroxymethylation have been proposed as potential mechanisms leading to DNA hypomethylation in lupus.
This article reviews current evidence for epigenetic abnormalities, and in particular DNA demethylation, in the pathogenesis of idiopathic and some forms of drug-induced lupus, and how impaired ERK pathway signaling may contribute to the development of human lupus through effects on T cell DNA methylation.
We therefore analyzed the PMA stimulated ERK pathway phosphorylation cascade in CD4(+) T cells from patients with lupus and in hydralazine-treated cells.
Whether the same genetic regulatory elements demethylate in T cells treated with Dnmt inhibitors, ERK pathway inhibitors, and in human lupus is unknown.