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Related Experiment Videos

Immunoadherence and complement in cancer-bearing mice.

C Porta, M L Villa, E Clerici

    British Journal of Cancer
    |January 1, 1978
    PubMed
    Summary
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    Tumor growth in mice reduces serum complement factors C3b and C3d, impairing immunoadherence. This suggests complement consumption via the alternative pathway during tumor-induced inflammation.

    Area of Science:

    • Immunology
    • Cancer Biology
    • Complement System

    Background:

    • Ehrlich ascites carcinoma (EAC) is a murine tumor model.
    • Immunoadherence assays assess complement system function.
    • The complement system plays a crucial role in immune responses.

    Purpose of the Study:

    • To investigate the effect of EAC tumor growth on serum complement levels.
    • To determine the impact of tumor growth on immunoadherence capacity.
    • To elucidate the complement pathway involved in tumor-associated immune modulation.

    Main Methods:

    • Grafting of Ehrlich ascites carcinoma cells into mice.
    • Measurement of serum complement components C3b and C3d concentrations.
    • Assessment of cellular receptor expression for complement factors.

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  • Analysis of complement pathway activation.

    • Main Results:

    • Tumor-bearing mice showed a significant decrease in serum C3b and C3d.
    • The capacity to mediate immunoadherence phenomena was lost shortly after tumor grafting.
    • Cellular receptors for C3b and C3d remained unaffected by tumor growth.
    • Evidence suggests activation of the alternative complement pathway.

    Conclusions:

    • Ehrlich ascites carcinoma growth leads to complement consumption.
    • The alternative complement pathway is likely activated during tumor-induced inflammation.
    • Complement system dysregulation may contribute to tumor progression.