Abstract
Background: L-selectin (CD62L) is a cell surface adhesion molecule recently shown to play a critical role in determining endometrial receptivity and implantation in humans. By contrast, the L-selectin ligand is missing from the rodent endometrium. Interestingly, CD62L (L-selectin)-deficient BALB/c mice delivered significantly higher numbers of viable offspring than wild type controls via mechanisms yet to be defined. Methods: Nulliparous CD62L-deficient (8-10-week-old, n = 25) or wild type (n = 18) females were mated with 43 age-matched males. Animals were sacrificed at gestational day (GD) 9.5. Tissue samples were analyzed by immunostaining and flow cytometry. Results: Mating wild type and CD62L-deficient BALB/c mice revealed that the increased birth rate was due to the CD62L deficiency in females. Flow cytometric analysis demonstrated significant differences in the number of natural killer (NK) cells present in the uterus of pregnant CD62L- deficient mice compared to controls. Immunohistochemistry confirmed NK cell accumulation at the fetal-maternal interface. Discussion: Uterine NK cells have been shown to peak at GD 8-10 at the fetal-maternal interface. NK cells might regulate mouse fertility rates by facilitating development of the maternal spiral arteries, thereby stimulating the formation of larger vessels that facilitate intrauterine survival, however, their role is not obligate to spiral artery development. Conclusions: Diminished CD62L expression modified immune cell trafficking into the uterus of pregnant mice generating a microenvironment primarily dominated by NK cells resulting in improved embryonic survival rates.
Highlights
Uterine implantation of the human embryo begins with attachment of the blastocyst to the trophoblast
To determine whether the L-selectin deficiency in either males or females was responsible for the observed increase in litter sizes and to determine the average number of viable pups, we performed a comparative breeding analysis using 10-week-old nulliparous BALB/c mice
CD62L-deficient females crossed with wild type (WT) males delivered 92 pups with an average number of 8.36 ± 0.77 standard error of the mean (SEM) pups/litter (Figure 1)
Summary
Uterine implantation of the human embryo begins with attachment of the blastocyst to the trophoblast. Because this process occurs under conditions of shear stress it parallels leukocyte transmigration, suggesting that the molecular basis of these processes might be analogous. CD62L plays a key first step in initiating leukocyte migration from specialized blood vessels (high endothelial venules) into the lymph node parenchyma following L-selectin binding to carbohydrate rich ligands. The same L-selectin adhesion system (L-selectin and its carbohydrate rich ligands) has been implicated in initial embryo-maternal interactions [4]-[6] and L-selectin/ligand binding has been suggested to be critical to uterine trophoblast cell development [7]. NK cells might regulate mouse fertility rates by facilitating development of the maternal spiral arteries, thereby stimulating the formation of larger vessels that facilitate
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
