作者: Jean-Marc Navenot , Marcello Villanova , Brigitte Lucas-H�ron , Alessandro Malandrini , Dominique Blanchard
DOI: 10.1002/(SICI)1097-4598(199701)20:1<92::AID-MUS12>3.0.CO;2-3
关键词:
摘要: Control of complement deposition on autologous cells is mediated by a group regulatory membrane proteins acting at different levels the cascade. Decay accelerating factor (CD55) prevents assembly C3 convertases and CD59 inhibitor reactive lysis (MIRL) restricts homologous attack complex (MAC) inhibition C5b-8 catalyzed insertion C9. The aim this work was to study eventual expression CD55 human skeletal muscle fibers. Highly sensitive immunoblotting using murine monoclonal antibodies showed that CD59, but not CD55, present in Immunocytochemistry with antibody against demonstrated dense granular immunostaining mainly localized level sarcolemma. Thus, expressed normal may play prominent role preventing MAC subsequent complement-mediated damage myopathies where system activation involved.