Hormonal Regulation of Complement Factor B in Human Endometrium
Version of Record online: 9 MAY 2013
American Journal of Reproductive Immunology
Volume 30, Issue 2-3, pages 63–67, September-October 1993
How to Cite
HASTY, L. A., BROCKMAN, W. W., LAMBRIS, J. D. and LYTTLE, C. R. (1993), Hormonal Regulation of Complement Factor B in Human Endometrium. American Journal of Reproductive Immunology, 30: 63–67. doi: 10.1111/j.1600-0897.1993.tb00603.x
- Issue online: 9 MAY 2013
- Version of Record online: 9 MAY 2013
- Accepted July 13, 1993
PROBLEM: Recent investigations have demonstrated the presence of complement components in human endometrium in a cycle-specific manner. Luteal phase endometrium has been shown to synthesize complement C3 de novo, whereas proliferative endometrium produces little or no C3. Likewise factor B. which is critical to the activation of the alternative pathway of complement, has been shown to be present only in the glandular epithelium of luteal phase endometrium. This investigation was designed to determine if factor B is present in the endometrium in a high progesterone state such as pregnancy or with exogenous progesterone treatment.
METHOD: Endometrial biopsies were obtained from patients on progesterone therapy. The endometrium of early pregnancy was evaluated by obtaining biopsies from patients with ectopic pregnancies as well as from patients undergoing therapeutic termination. Immunohistochemistry was performed on each biopsy using monoclonal antibodies to factor B.
RESULTS: Our results demonstrate the presence of factor B in the glandular epithelial cells of the endometrium of patients treated with exogenous progesterone therapy. Additionally. factor B was localized to the glandular compartment of the endometrium from patients with ectopic gestations. Interestingly, the evaluation of an implantation site from an early gestation demonstrated factor B in the maternal decidua only; trophoblast did not exhibit the presence of factor B.
CONCLUSION: Factor B exists in the endometrium in a hormone-dependent manner and is not expressed in fetal tissue in early gestation.