Expression of CD59, a human complement system regulatory protein, in extraembryonic membranes
O A Vanderpuye1, C A Labarrere, J A McIntyre
1Center for Reproduction and Transplantation Immunology, Methodist Hospital of Indiana, Inc., Indianapolis 46202.
International Archives of Allergy and Immunology
|January 1, 1993
Summary
Leukocyte cluster of differentiation antigen 59 (CD59) protects cells from complement damage. This study found CD59 is present in human pregnancy tissues, suggesting a role in protecting the fetus from maternal immune attack.
Area of Science:
- Immunology
- Reproductive Biology
- Cell Biology
Background:
- The terminal complement system can cause cell lysis.
- CD59 (leukocyte cluster of differentiation antigen 59) is a key complement regulatory protein.
- Understanding complement regulation in pregnancy is crucial.
Purpose of the Study:
- To characterize the expression and function of CD59 in human extraembryonic membranes.
- To investigate the role of CD59 in protecting fetal tissues during pregnancy.
Main Methods:
- Immunohistochemistry using CD59 monoclonal antibody MEM-43.
- Immunoblotting and ELISA to analyze CD59 in syncytiotrophoblast microvilli (STM).
- Comparison of CD59 expression in normal and pathological pregnancy states.
Main Results:
- CD59 was detected on the apical surface of syncytiotrophoblast, extravillous cytotrophoblast, and amniotic epithelium.
- STM contains a CD59 glycoprotein with similar mass and glycosylation to adult tissues.
- STM showed significantly higher reactivity with MEM-43 than other tissues.
- CD59 expression in term placental STM was similar in normal and post-immunotherapy recurrent spontaneous abortion patients.
- Plasma from pregnant women and umbilical cords exhibited higher CD59 reactivity.
Conclusions:
- CD59 is expressed in human extraembryonic membranes, suggesting a protective role against complement-mediated damage.
- Its apical localization supports functional polarization and immunological roles in the syncytiotrophoblast.
- CD59 may protect extraembryonic epithelia from complement attack in maternal blood and amniotic fluid.
