The intracellular 52‐kd Ro/SSA autoantigen in keratinocytes is up‐regulated by tumor necrosis factor α via tumor necrosis factor receptor I

Inhibition of Autoantigen Expression by (-)-Epigallocatechin-3-gallate (the Major Constituent of Green Tea) in Normal Human Cells

“…The pathogenesis of most autoimmune disorders, including systemic lupus erythematosus (SLE) and Sjö-gren's syndrome (SS), remains incompletely understood (Yamamoto, 2003;Venables, 2004). SLE and SS are characterized by the production of autoantibodies against normal cellular components, designated as autoantigens, that may be overexpressed (Gerl et al, 2005). The production of autoantibodies is considered to be a key mechanism of pathogenesis.…”

New insights into the pathogenesis of systemic lupus erythematosus

“…TNF-α is produced not only by macrophages but also by keratinocytes in the skin after UVB exposure. In a study exploring TNF-α effect on cells, it is shown that TNF-α can induce the production of the 50 kd Ro protein and mRNA [35]. Since Ro protein (antigen) is expressed on apoptotic bodies and anti-Ro antibodies are associated with cutaneous lupus, TNF-α may play a major role in UVB-induced skin disease in SLE.…”

Clinical perspectives and murine models of lichenoid tissue reaction/interface dermatitis

“…On the other hand, cell-surface Ro/SSA antigen expressed on keratinocytes, which is upregulated by an exposure of ultraviolet radiation or by tumor necrosis factor (TNF)-a stimulation, is associated with CLE, especially SCLE [5]. In keratinocytes from patients with neonatal lupus erythematosus (NLE), the expression of Ro/SSA and La/SSB molecules is upregulated as targets, and sera derived from the NLE patient or his mother exhibited a cytotoxic effect on the keratinocytes [6].…”