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Related Experiment Videos

Early embryonic cells activate the alternative complement system

R Kircheis1, L Kircheis, H Oshima

  • 1Biotechnology Research Center, Teikyo University, Kawasaki, Japan.

In Vivo (Athens, Greece)
|March 1, 1995
PubMed
Summary

Embryonic cells are highly sensitive to complement-mediated lysis via the alternative complement system (ACS). Low sialic acid and specific complement regulatory protein expression on these cells contribute to their vulnerability.

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Area of Science:

  • Immunology
  • Developmental Biology
  • Cell Biology

Background:

  • Matured cells exhibit resistance to cytolysis by normal human serum.
  • Embryonic cells, including stem cells and carcinoma cells, show extreme sensitivity to serum-induced lysis.
  • This sensitivity is distinct from lysis observed in more differentiated cells.

Purpose of the Study:

  • To investigate the mechanism behind the heightened sensitivity of embryonic cells to serum-mediated cytolysis.
  • To determine which complement activation pathway is involved in the lysis of embryonic cells.
  • To explore the role of complement regulatory proteins and cell surface molecules in this process.

Main Methods:

  • Treatment of embryonic cells with normal human serum under various complement pathway blocking conditions (classical and alternative).

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  • Analysis of complement regulatory protein expression (Crry, Cr2) via mRNA.
  • Quantification of membrane-bound sialic acid levels on embryonic versus adult cells.

    • Main Results:

    • Embryonic cells activate the alternative complement system (ACS), as blocking this pathway abrogated lysis, while blocking the classical pathway did not.
    • Cytotoxicity was confirmed using syngeneic murine serum, indicating an conserved mechanism.
    • Embryonic cells express Crry and uniquely express Cr2 transcripts, and possess significantly lower membrane-bound sialic acid levels compared to adult cells.

    Conclusions:

    • Embryonic cells are susceptible to complement-mediated lysis primarily through the alternative complement system.
    • The low expression of membrane-bound sialic acid and the specific expression profile of complement regulators (Crry, Cr2) contribute to this vulnerability.
    • These findings shed light on the innate immune interactions with early developmental cells.