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Decay-accelerating factor protects human trophoblast from complement-mediated attack
1Department of Obstetrics and Gynecology, National Naval Medical Center, Bethesda, Maryland 20889-5000.
Clinical Immunology and Immunopathology
|February 1, 1995
Summary
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.
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.