Together, these results support a model in which oxidative stress contributes to the development of autoantibodies in lupus, Sjogren’s Syndrome and possibly other inflammatory diseases by inactivating T cell PKCδ through nitration, decreasing ERK pathway signaling and Dnmt1 levels, epigenetically altering gene expression in a subset of CD4+ T cells. The gene discussed is PRKCD; the disease is Sjogren syndrome.