RAISED ANTIENDOTHELIAL CELL AUTOANTIBODIES (AECA), BUT NOT ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES (ANCA), IN RECURRENT ORAL ULCERATION -MODULATION OF AECA BINDING BY TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA)AND INTERFERON-GAMMA (IFN-GAMMA)

Recurrent oral ulceration (ROU) is a common oral mucosal condition of unknown etiology. However, there is evidence to suggest that vasculiti s may play a role. Here we investigate the presence in ROU of two auto antibodies associated with vasculitis, AECA and ANCA. AECA target as y et unidentified antigens on the endothelial cell surface and have been identified in patients with vasculitic disorders and inflammatory con ditions with a vasculitic component. ANCA target specific neutrophil-a ssociated proteins and are detected in specific vasculitic and chronic inflammatory disorders. AECA and ANCA levels were studied in 20 ROU p atients and 20 controls. IgG AECA to the endothelial cell line ECV 304 were detected in 19 ROU patients and four controls. Levels were signi ficantly raised in ROU both to ECV 304 (P < 0.000 05) and to human umb ilical vein endothelial cells (HUVEC) (P < 0.005). Although levels wer e highest during episodes of ulceration, they were also raised between episodes. Stimulation of endothelial cells with TNF-alpha significant ly increased AECA binding of both ROU (P < 0.005) and control samples (P < 0.0001), while IFN-gamma decreased binding (ROU P < 0.0001; contr ols P < 0.05). In contrast, ANCA were detected in only one patient and none of the controls. The presence of raised levels of AECA lends sup port to the hypothesis that a vasculitic process may underlie ROU. Mor eover, these findings suggest that endothelial cell expression of AECA target antigens is increased by TNF-alpha and decreased by IFN-gamma stimulation.