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CD59 efficiently protects human NT2-N neurons against complement-mediated damage.

E D Pedersen1, H C D Aass, T Rootwelt

  • 1Institute of Immunology, Rikshospitalet HF, University of Oslo, Oslo, Norway. pedersen@medisin.uio.no

Scandinavian Journal of Immunology
|July 20, 2007
PubMed
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The complement regulatory protein CD59 protects human neurons from cell death. Blocking CD59 on neurons triggers complement-mediated damage and neuronal loss, highlighting CD59

Area of Science:

  • Neuroimmunology
  • Complement System Biology
  • Cellular Stress Response

Background:

  • The complement regulatory protein CD59 prevents terminal complement complex (C5b-9) formation on cell membranes, protecting cells from lysis.
  • Loss of CD59 function increases cellular susceptibility to complement-mediated damage.
  • Immunoglobulin M (IgM) deposition can initiate complement activation, leading to cell death, particularly relevant in neurological conditions.

Purpose of the Study:

  • To investigate the functional role of CD59 in protecting human NT2-N neurons against IgM-mediated complement activation and subsequent cell death.
  • To determine if CD59 is essential for neuronal survival during complement attack.

Main Methods:

  • NT2-N neurons were incubated with IgM monoclonal antibody A2B5 to induce complement activation.

Related Experiment Videos

  • Complement activation was assessed by detecting C1q and C5b-9 deposition on cell membranes and soluble C5b-9 (sC5b-9) in supernatants.
  • CD59 function was inhibited using the monoclonal antibody BRIC 229; complement activation was blocked using compstatin (C3 inhibitor) and anti-C5/C5a monoclonal antibodies.
  • Cell membrane damage was evaluated using propidium iodide staining and immunofluorescence microscopy; neuronal process degeneration was assessed with crystal violet staining.

    • Main Results:

    • Incubation with A2B5 antibody and human serum induced complement activation on NT2-N neurons, evidenced by C1q deposition.
    • Blocking CD59 with MoAb BRIC 229 led to significant C5b-9 deposition, cell death, and axonal degeneration.
    • Inhibition of complement activation via compstatin or anti-C5 antibodies effectively prevented neuronal damage.
    • Control IgM antibody and isotype-matched control antibody for BRIC 229 did not induce significant complement-mediated damage.

    Conclusions:

    • CD59 is crucial for protecting human NT2-N neurons from complement-mediated damage induced by IgM activation.
    • The findings suggest that CD59 deficiency or dysfunction could contribute to neuronal injury in clinical conditions like stroke.