Ts. Jensen et al., IDENTIFICATION OF THE COMPLEMENT REGULATORY PROTEINS CD46, CD55, AND CD59 IN HUMAN FALLOPIAN-TUBE, ENDOMETRIUM, AND CERVICAL MUCOSA AND SECRETION, American journal of reproductive immunology [1989], 34(1), 1995, pp. 1-9
PROBLEM: Complement lytic activity has been demonstrated, and a potent
ial for its activation is present in human cervical and tubal secretio
ns and in the endometrium. This necessitates the presence of regulator
y 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 fo
r 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 u
ndergoing hysterectomy for benign conditions, and specimens were selec
ted from different stages of the menstrual cycle. Fallopian tubes were
obtained from patients submitted for sterilization, while cervical mu
cus was aspirated from volunteers undergoing gynecological examination
. Immunohistochemistry was performed on all tissue samples, using mono
clonal antibodies to membrane cofactor protein (MCP), decay accelerati
ng factor (DAF), CD59 and complement receptor 1 (CR1). Western blot an
alysis was performed on cervical mucus under nonreducing conditions. R
ESULTS: MCP, DAF, and CD59 were found to be expressed in human endomet
rium and fallopian tube. No variation in expression was detected throu
ghout 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 through
out the female genital tract, and may thus play an important role in p
rotecting the traversing sperm and implanting blastocyst from compleme
nt mediated damage.