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Decay-accelerating factor protects human tumor cells from complement-mediated cytotoxicity in vitro.

N K Cheung¹, E I Walter, W H Smith-Mensah

¹Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York 10021.

The Journal of Clinical Investigation

|April 1, 1988

Summary

The decay-accelerating factor (DAF) protects some melanomas from complement-mediated killing. Blocking DAF enhances tumor cell lysis, suggesting a therapeutic target for immunotherapy against GD2-expressing cancers.

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Area of Science:

Immunology
Oncology

Background:

Disialoganglioside GD2 is a target antigen on various human tumors, including neuroblastomas and melanomas.
Monoclonal antibody 3F8 binding to GD2 mediates complement-dependent cytotoxicity, but sensitivity varies between tumor types.

Purpose of the Study:

To investigate the mechanism of complement-mediated cytotoxicity resistance in GD2-positive melanoma cell lines.
To determine the role of decay-accelerating factor (DAF) in differential complement sensitivity.

Main Methods:

Comparison of DAF expression in complement-sensitive neuroblastomas and complement-insensitive melanomas.
Blocking DAF function using anti-DAF monoclonal antibodies (MAbs) and F(ab')2 fragments.
Assessment of C3 uptake and complement-mediated lysis in melanoma cell lines.

Main Results:

DAF was undetectable in neuroblastomas but present in complement-insensitive melanomas.
Blocking DAF function significantly enhanced C3 uptake and complement-mediated lysis in insensitive melanoma lines.
Both intact anti-DAF MAb and F(ab')2 fragments effectively sensitized melanoma cells to complement attack.

Conclusions:

DAF expression confers resistance to complement-mediated killing in some GD2-positive melanomas.
Targeting DAF function represents a potential strategy to enhance immunotherapy efficacy against these tumors.