Expression of CD59, a regulator of the membrane attack complex of complement, on human skeletal muscle fibers

• Published in: Muscle & nerve Vol. 20; no. 1; pp. 92 - 96
• Main Authors: Navenot, Jean-Marc, Villanova, Marcello, Lucas-Héron, Brigitte, Malandrini, Alessandro, Blanchard, Dominique, Louboutin, Jean-Pierre
• Format: Journal Article
• Language: English
• Published: New York John Wiley & Sons, Inc 01.01.1997; Wiley
• Subjects: Biological and medical sciences; CD55 Antigens - pharmacology; CD59; CD59 Antigens - metabolism; complement; Complement Membrane Attack Complex - metabolism; Fundamental and applied biological sciences. Psychology; Humans; Immunohistochemistry; membrane attack complex; muscle fibers; Muscle, Skeletal - metabolism; Striated muscle. Tendons; Vertebrates: osteoarticular system, musculoskeletal system; Antigen; Human; Membrane attack complex; Complement; Muscular fiber; Gene expression; Striated muscle; Myopathy
• ISSN: 0148-639X; 1097-4598
• DOI: 10.1002/(SICI)1097-4598(199701)20:1<92::AID-MUS12>3.0.CO;2-3

Control of complement deposition on autologous cells is mediated by a group of complement regulatory membrane proteins acting at different levels of the complement cascade. Decay accelerating factor (CD55) prevents the assembly of C3 convertases and CD59 membrane inhibitor of reactive lysis (MIRL) restricts homologous complement lysis by the membrane attack complex of complement (MAC) by inhibition of C5b‐8 catalyzed insertion of C9. The aim of this work was to study the eventual expression of CD55 and CD59 on human skeletal muscle fibers. Highly sensitive immunoblotting using murine monoclonal antibodies showed that CD59, but not CD55, was present in skeletal muscle fibers. Immunocytochemistry with a monoclonal antibody against CD59 demonstrated a dense granular immunostaining mainly localized at the level of the sarcolemma. Thus, CD59, but not CD55, is expressed on normal skeletal muscle fibers. CD59 may play a prominent role in preventing MAC deposition and subsequent complement‐mediated damage in myopathies where the complement system activation is involved. © 1997 John Wiley & Sons, Inc.