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Human carcinomas variably express the complement inhibitory proteins CD46 (membrane cofactor protein), CD55
G A Niehans1, D L Cherwitz, N A Staley
1Pathology and Laboratory Medicine Service, Minneapolis Veterans Affairs Medical Center, MN, USA.
The American Journal of Pathology
|July 1, 1996
Summary
Most human carcinomas express complement inhibitors, like decay-accelerating factor (DAF) and CD59, to evade immune attack. Some tumors release these proteins into the stroma, suggesting a novel protective mechanism against complement-mediated damage.
Area of Science:
- Immunology
- Oncology
- Cell Biology
Background:
- Normal tissues utilize membrane-bound complement inhibitory proteins to prevent autologous complement system damage.
- Neoplasms may alter expression of these protective proteins, potentially impacting their susceptibility to complement-mediated lysis.
Purpose of the Study:
- To investigate the expression patterns of complement inhibitors (DAF, CD59, MCP) in various human carcinomas.
- To assess the deposition of complement components (C3 fragments, C5b-9) in neoplastic versus non-neoplastic tissues.
- To explore potential differences in inhibitor expression between normal tissues and corresponding tumors.
Main Methods:
- Immunohistochemistry was employed to examine frozen tissue samples of human breast, colon, kidney, and lung carcinomas.
- Analysis included assessing the distribution of decay-accelerating factor (DAF), CD59 (protectin), and membrane cofactor protein.
- Complement activation products, C3 fragments and C5b-9, were also evaluated for deposition.
Main Results:
- Significant variations in complement inhibitor expression were observed across different carcinoma types and between tumors and normal tissues.
- Breast ductal carcinomas exhibited diverse phenotypes, while colon carcinomas showed strong expression of all inhibitors.
- Lung small cell carcinomas displayed minimal inhibitor expression, contrasting with other examined neoplasms that generally expressed one or more inhibitors.
Conclusions:
- Most carcinomas, excluding small cell lung cancer, express complement inhibitors, likely to resist complement-mediated damage.
- Tumor stroma frequently contained high levels of DAF and CD59, suggesting carcinomas may release soluble forms of these inhibitors.
- This extracellular release may represent an additional mechanism for carcinomas to evade complement attack.