Protectin (CD59) inhibits homologous complement-mediated cytolysis by preventing formation of the membrane attack complex at the point of insertion and polymerization of C9 into cell membranes. The present study investigated the expression and function of CD59 on human prostatic tumor cells in situ
Expression of CD59, a regulator of the membrane attack complex of complement, on human skeletal muscle fibers
✍ Scribed by Jean-Marc Navenot; Marcello Villanova; Brigitte Lucas-Héron; Alessandro Malandrini; Dominique Blanchard; Jean-Pierre Louboutin
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 158 KB
- Volume
- 20
- Category
- Article
- ISSN
- 0148-639X
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✦ Synopsis
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.
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