Identification of the Complement Regulatory Proteins CD46, CD55, and CD59 in Human Fallopian Tube, Endometrium, and Cervical Mucosa and Secretion


Broegelmann Research Laboratory for Microbiology, Armauer Hansen Building, N-5021 Bergen, Norway.


PROBLEM: Complement lytic activity has been demonstrated, and a potential for its activation is present in human cervical and tubal secretions and in the endometrium. This necessitates the presence of regulatory mechanisms for protection of the sperm and the implanting allogeneic conceptus in the female genital tract. Complement regulatory proteins demonstrated on sperm and in seminal fluid have been attributed such a role. It is however likely that additional protection is required for a successful conception and implantation to take place. This lead us to investigate the distribution of the complement regulatory factors in cervical mucus and mucosa, uterine endometrium, and fallopian tube.

METHOD: Endometrium and cervical mucosa were obtained from patients undergoing hysterectomy for benign conditions, and specimens were selected from different stages of the menstrual cycle. Fallopian tubes were obtained from patients submitted for sterilization, while cervical mucus was aspirated from volunteers undergoing gynecological examination. Immunohistochemistry was performed on all tissue samples, using monoclonal antibodies to membrane cofactor protein (MCP), decay accelerating factor (DAF), CD59 and complement receptor 1 (CR1). Western blot analysis was performed on cervical mucus under nonreducing conditions.

RESULTS: MCP, DAF, and CD59 were found to be expressed in human endometrium and fallopian tube. No variation in expression was detected throughout the menstrual cycle. CR1 was not expressed. Soluble forms of DAF and CD59 were found to be present in cervical mucus.

CONCLUSION: The complement regulatory proteins MCP, DAF, and CD59 are expressed throughout the female genital tract, and may thus play an important role in protecting the traversing sperm and implanting blastocyst from complement mediated damage.