Demonstration of the Presence of IL-16, IL-17 and IL-18 at the Murine Fetomaternal Interface during Murine Pregnancy
Version of Record online: 21 FEB 2003
American Journal of Reproductive Immunology
Volume 49, Issue 2, pages 101–112, February 2003
How to Cite
Ostojic, S., Dubanchet, S., Chaouat, G., Abdelkarim, M., Truyens, C. and Capron, F. (2003), Demonstration of the Presence of IL-16, IL-17 and IL-18 at the Murine Fetomaternal Interface during Murine Pregnancy. American Journal of Reproductive Immunology, 49: 101–112. doi: 10.1034/j.1600-0897.2003.01150.x
- Issue online: 21 FEB 2003
- Version of Record online: 21 FEB 2003
- Submitted October 2, 2001; revised December 28, 2001; accepted December 31, 2001.
- Th1/Th2 paradigm
PROBLEM: To determine if interleukin-16 (IL-16), IL-17, and IL-18 are present at the murine fetomaternal interface during pregnancy as a first step towards investigating their roles in fetomaternal relationship.
METHODS: Expression of IL-16, IL-17, and IL-18, was assessed by immunohistochemistry (IHC) in the BALB/c × BALB/k (H2d × H2k), and the CBA/J × BALB/c non-abortion prone, and CBA/J × DBA/2 abortion prone matings. Enzyme-linked immunosorbent assay (ELISA) were performed for the two latter cytokines to compare local production in the abortion prone CBA/J × DBA/2 versus the non-abortion prone CBA/J × BALB/c matings.
RESULTS: Expression of IL-17 was borderline. The anti-IL-16 staining specifically localized in the uterine stroma and glandular epithelium and was rather low in the placenta. IL-18 staining started in the peri-implantation uterus in the basal proliferative stroma, and was also traced, although weaker, in the glandular epithelium. In the immediate post-implantation period, a weak stromal staining persisted but there was a strong labeling of the ectoplacental cone. Interestingly, when the ectoplacental cone differentiates into placenta having a major histocompatibility complex (MHC) class I+ spongiotrophoblast and a (MHC class I–) labyrinth, a very strong transient labeling of uterine natural killer (u-NK) cells was found. Later in gestation, IL-18 was also produced by giant cell and spongiotrophoblast. Finally, we compared by ELISA the production of IL-17/-18 in CBA/J × DBA/2 and CBA/J × BALB/c matings. We detected significantly more IL-18 in the non-abortion prone combination decidua or placenta.
CONCLUSION: The three cytokines IL-16, IL-17, and IL-18 were detected at the fetomaternal interface with a tissue specific, stage-dependent distribution. The predominance of IL-18 secretion in the non-resorption prone matings lead us to question the general validity of the classical T-helper (Th)1/2 paradigm.