Systemic Lupus Erythematosus is an autoimmune disease, it could be multi-systemic and characterized by auto-antibodies, especially antinuclear (anti-Ro, anti-La, anti-DNA), damage is mediated by immune complexes. The injuries in the skin of patients with SLE are aggravated by sun exposition (UV light and heat), altering the cellular expression and distribution of Ro60 antigen. In order to understand the damage mechanism involved in skin of patients with LES by environmental stressors, we developed a murine model focused in Ro60 and the heat shock proteins family (Hsp) expression. Objective: Determinate the cellular damage of the skin of newborn Balb/c mice, which was measured through the expression of the Ro60, Hsp27, 60, 70 and 90. Methods: Balb/c mice were exposed to different physical and chemical stressors like UV irradiation, heat (40ºC), H2O2, ethanol, HgCl2, camptotecine and cicloheximide drugs, in presence or absence of caspase 3 inhibitor. Skin extracts were obtained and the proteins Hsp27, 60, 70 and 90 were characterized and immunodetected by PAGE-SDS and Western blot using ECL, densytometric analysis was performed. Results: The Ro60 expression is modified with physical and chemical stressors, also it is increased mainly with UV light and heat, and decreased with caspase 3 ihnibitor. Hsp27, Hsp70, Hsp90 was similar to Ro60. The over expression of those proteins during the stress have the same profile. However using caspase 3 inhibitors before the stress, a down regulation are observed.