ABSTRACT
El Síndrome de Evans es un desorden heterogéneo caracterizado por el desarrollo simultáneo o secuencial de trombocitopenia autoinmune y anemia hemolítica autoinmune. Esta enfermedad de curso crónico ha sido correlacionada con inmunodeficiencias primarias, enfermedades colágeno-vasculares, desórdenes linfoproliferativos, y síndromes linfoproliferativos auto inmunes (ALPS). Los nuevos conceptos en su patogénesis aumentan el campo de investigación clínica del paciente, y constituyen el punto de partida para futuras terapias.
Evans syndrome is a heterogeneous disorder characterized by simultaneous development and sequence of autoimmune thrombocytopenia and autoimmune hemolytic anemia. This disease of chronic course has been correlated with primary immunodeficiency, collagen- vascular diseases, linfoproliferative disorders, and autoimmune linfoproliferative syndromes (ALPS). The news concepts in his pathogenesis increase the field of clinic investigation of the patient, and constitute the point to begin future therapies.
Subject(s)
Adult , Female , Anemia, Hemolytic , Autoimmune Diseases , Thrombocytopenia , PancytopeniaABSTRACT
AIM: To determine the role of Fas antigen and caspase-8 in modulating apoptosis of osteosarcoma cells induced by bacterial redox protein azurin. METHODS: The human osteosarcoma cell line U2OS was treated with bacterial redox protein azurin (150 mg/L) for 6, 12, 24 and 48 h, respectively. Cell immunohistochemistry and quantitative image pattern analysis were applied for detecting the expression of Fas antigen. Caspase-8 activity was detected using caspase-8 fluorescent assay kit. The apoptotic rate was measured by FCM. RESULTS: Compared with the control group, the expression of Fas antigen and activity of caspase-8 significantly increased in U2OS cells treated with 150 mg/L azurin (P