Caspase 3 blocking avoids the expression of autoantigens triggered by apoptosis in neonatal Balb/c mice skin

Abstract

Apoptosis is a physiologic process that maintains the cellular exchange; normally the cellular remains are cleared by phagocytosis without infl ammation. In autoimmunity defects in apoptosis may occur, which play an important role in pathogenesis. During the lymphoid ontogeny the failure of the Fas pathway could decrease the negative selection process and such defect could allow the survival of autoimmune lymphocyte clones resulting in a central tolerance breaking down; in other instances the peripheral tolerance is disrupted by an insuffi cient clearance of apoptotic material, which is a potential risk for activating the pre-existent auto-reactive clones.