Leukocytes are migratory cells. Highly specialized and regulated mechanisms exist to control their extravasation from the blood into tissues. Specificity for particular organs and tissues is provided by tissue-selective expression of vascular adhesion ligands and by tissue-selective chemoattractant factors. The successful coexistence of semiallogeneic cells at the maternal/fetal interface suggests that the pregnant uterus represents an environment in which leukocyte trafficking needs to be exquisitely regulated to establish a selected population of maternal leukocytes that support, modulate and regulate trophoblast invasion and local immunity. Especially during the critical period of initial placenta development in the mouse, there is an elegantly orchestrated progression of leukocyte homing events in the decidua basalis associated with the segregation of the major infiltrating leukocyte subsets into distinct decidual microenvironments. Switches of vascular addressins during the course of pregnancy parallel changes in the population of recruited leukocytes and transform the leukocyte-rich mid-term decidua basalis into the relatively leukocyte-poor phenotype at term. However, these mechanisms are sensitive to disruption. Consequently, it is relevant to understand how these mechanisms are modulated during abnormal pregnancy, where a dramatically altered decidual leukocyte composition may be involved in fetal loss.