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Complement membrane attack complexes induce in human leukemic cells rapid expression of large proteins (L-CIP).

Y Reiter1, Z Fishelson

  • 1Department of Chemical Immunology, Weizmann Institute of Science, Rehovot, Israel.

Molecular Immunology
|June 1, 1992
PubMed
Summary

Sublytic doses of complement membrane attack complexes (MAC) trigger rapid synthesis of large complement-induced proteins (L-CIP) in human leukemic cells. This response, mediated by MAC, highlights a potential mechanism for leukemic cell resistance to complement-mediated damage.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • The complement system is a crucial part of innate immunity, but its role in modulating cellular processes in cancer cells is not fully understood.
  • Membrane attack complexes (MAC) are terminal components of the complement cascade, typically leading to cell lysis.
  • Leukemic cells exhibit varying sensitivity to complement-mediated damage, suggesting underlying protective mechanisms.

Purpose of the Study:

  • To investigate the effect of sublytic doses of complement membrane attack complexes (MAC) on protein synthesis in human leukemic cells.
  • To identify and characterize novel proteins induced by MAC in leukemic cells.
  • To elucidate the role of MAC-induced protein synthesis in leukemic cell resistance to complement-mediated damage.

Main Methods:

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  • K562 erythroleukemic cells were treated with sublytic doses of complement from various sera (human, rabbit, guinea pig).
  • Protein synthesis was analyzed using SDS-PAGE and autoradiography following incorporation of radiolabeled amino acids ([35S]-Met, [3H]-Leu).
  • Antibodies against induced proteins were generated for immunoassay and immunofluorescence; effects of protein and RNA synthesis inhibitors were assessed.

Main Results:

  • Sublytic MAC treatment rapidly induced the synthesis of high molecular weight proteins (large complement-induced proteins, L-CIP) in K562 cells.
  • L-CIP synthesis was dependent on active complement MAC formation, requiring functional C7 and C8, and was inhibited by cycloheximide and actinomycin D.
  • L-CIP were also induced in U937 and HL-60 cells but not in a complement-sensitive K562 subline, suggesting a role in resistance.

Conclusions:

  • Sublytic MAC engagement triggers a specific protein synthesis response (L-CIP) in certain human leukemic cells.
  • This L-CIP induction is a MAC-dependent phenomenon and appears to be associated with cellular resistance to complement-mediated immune damage.
  • The findings suggest that leukemic cells may utilize induced protein synthesis as a survival mechanism against complement attack.