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

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

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

E D Pedersen,H C D Aass,T Rootwelt,M Fung,J D Lambris,T E Mollnes,

The complement regulatory protein CD59 controls cell survival by the inhibition of C5b-9 formation on the cell membrane. Loss of CD59 increases the susceptibility of cells to complement-mediated damage and lysis. Deposition of IgM can induce complement activation with subsequent cell death. We have previously demonstrated the presence of CD59 on human NT2-N neurons. In this study, we investigated the functional role of CD59 for NT2-N cell survival after IgM-mediated complement activation. Complement activation was induced on NT2-N neurons with human serum following incubation with the IgM monoclonal antibody A2B5 reacting with a neuronal cell membrane epitope. Deposition of C1q and C5b-9 was detected on the cell membrane and sC5b-9 in the culture supernatant. Specific inhibition of complement was obtained by the C3 inhibitor compstatin, and by anti-C5/C5a MoAb. CD59 was blocked by the MoAb BRIC 229. Membrane damage of propidium iodide-stained NT2-N cells was confirmed by immunofluorescence microscopy and degeneration of neuronal processes was shown with crystal violet staining. A2B5, but not the irrelevant control IgM antibody, induced complement activation on NT2-N neurons after incubation with a human serum, as detected by the deposition of C1q. A marked membrane deposition of C5b-9 on NT2-N neurons with accompanying cell death and axonal degeneration was found after the blocking of CD59 with MoAb BRIC 229 but not with an isotype-matched control antibody. Compstatin and anti-C5 monoclonal antibodies which blocked C5 activation efficiently inhibited complement activation. In conclusion, CD59 is essential for protecting human NT2-N neurons against complement-mediated damage, which is known to occur in a number of clinical conditions including stroke.

CD59 efficiently protects human NT2-N neurons against complement-mediated damage. Publishing Authors By Initials

ED Pedersen,HC Aass,T Rootwelt,M Fung,JD Lambris,TE Mollnes,

For similar nervous system: neurons research abstracts see: nervous system: neurons research

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

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Scandinavian journal of immunology

VOLUME: 66

Page Numbers: 345-51

Journal Abbreviation: Scand. J. Immunol.

ISSN: 0300-9475

DAY: 3

MONTH: 12

YEAR: 2007

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

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LANGUAGE: eng

NlmUniqueID: 323767

CD59 efficiently protects human NT2-N neurons against complement-mediated damage. Keywords Mesh Terms:

KEYWORDS: Neurons

MESH TERMS: pathology

Chemical & Substance for Abstract: CD59 efficiently protects human NT2-N neurons against complement-mediated damage. Information

Substance Name: CD59 protein, human

Registry Number: 101754-01-2

Grant and Affiliation Information for CD59 efficiently protects human NT2-N neurons against complement-mediated damage.

AFFILIATION: Institute of Immunology, Rikshospitalet HF, University of Oslo, Oslo, Norway. pedersen@medisin.uio.no

Country: England

AGENCY: United States NIGMS

GRANT: GM62134

ACRONYM: GM

MEDLINETA: Scand J Immunol

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