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Decay-accelerating factor protects human trophoblast from complement-mediated attack

D S Cunningham1, J R Tichenor

  • 1Department of Obstetrics and Gynecology, National Naval Medical Center, Bethesda, Maryland 20889-5000.

Clinical Immunology and Immunopathology
|February 1, 1995
PubMed
Summary
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Recurrent pregnancy loss may involve low complement levels. Trophoblasts use decay-accelerating factor (DAF) to evade the complement system, suggesting immunotherapy potential for recurrent spontaneous aborters.

Area of Science:

  • Immunology
  • Reproductive Biology
  • Biochemistry

Background:

  • Approximately 20% of first-trimester pregnancy losses are preceded by hypocomplementemia.
  • Trophoblasts are crucial for early pregnancy, and their interaction with the maternal immune system is key.

Purpose of the Study:

  • To investigate the role of decay-accelerating factor (DAF) in trophoblast immune evasion.
  • To explore the potential of DAF as a therapeutic target for recurrent spontaneous abortion.

Main Methods:

  • Monoclonal antibodies against DAF were used to assess DAF levels on trophoblastic tissues.
  • Complement activation via the alternate C' pathway (ACP) was studied using normal human sera and trophoblastic tissues.
  • Phospholipase C was used to investigate the membrane anchoring of DAF.

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Main Results:

  • Trophoblastic tissues from hypocomplementemic women had significantly lower DAF levels (approx. 10%) compared to normocomplementemic women.
  • Anti-DAF antibodies induced complement activation on normocomplementemic trophoblastic tissue via the ACP.
  • Phospholipase C treatment of normocomplementemic trophoblastic tissue led to serum decomplementation.

Conclusions:

  • Trophoblasts appear to evade the ACP through functional DAF, likely via its membrane-anchored moiety.
  • These findings suggest immunotherapy targeting DAF could be a viable treatment for recurrent spontaneous abortion.