Intracellular antigens released from Balb/c mice kidneys under chemically induced apoptosis and/or necrosis

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Apoptosis is a physiologic process that makes certain the cellular exchange; after apoptosis cellular corpses are cleared by phagocytosis. In autoimmunity, some mechanisms of apoptosis are not succeeding and result in autoimmunity; for instance the failure in the Fas pathway in lymphoid ontogeny fosters the autoimmune clone survival. Additionally the insufficient clearance of apoptotic material represents a potential danger that may activate the pre-existent auto-reactive clones, and may trigger the autoantibody production (1). Is now accepted that antigens from apoptotic origin are better targeted by autoantibodies (2-4), and the source of apoptotic remains is broad spread, nevertheless the skin is very important because is an easy target of the UV light, and may induce antibody deposition\resulting in skin lesions, this mechanism is important in SCLE (5).

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Ramírez-Sandoval, R., Vázquez-del-Mercado, M., Daneri-Navarro, A., López-Robles, E., Bollain-y-Goitia, J., Avalos-Diaz, E., & Herrera-Esparza, R. (2008). Intracellular antigens released from Balb/c mice kidneys under chemically induced apoptosis and/or necrosis. Reumatismo, 60(2), 108–113. https://doi.org/10.4081/reumatismo.2008.108