The placental RCAS1 expression during stillbirth

Dynamic fetal growth observed between 20th and 28th week of pregnancy is accompanied by fetal maturation which enables further uncomplicated extra-uterine growth. The fetal development is possible due to the phenomenon of maternal immunological tolerance to fetal antigens. Severe disturbances of the fetal growth might in some cases result in fetal intrauterine death. Some of the most common fetal death causes constituting about 50% of all cases include placental maturation disorders and fetal congenital malformations [1]. Stillbirth may be considered a form of complicated vaginal labor. Independently of the fetal death cause the beginning and course of stillbirth is closely related to the growing cytotoxic activity at the maternal-fetal interface. However, this activity does not have to arise simultaneously with the fetal death. In some situations fetal death may not be accompanied by immediate clinical features of the onset of labor. Molecular changes in membrane proteins expressed by trophoblast cells usually lead to the beginning of normal term delivery but may also be found in stillbirth. These proteins are neccessary for the development of maternal immune tolerance phenomenon. Cellular membrane proteins expressed by trophoblast cells that seem to be responsible for suppressing CTLs, dNK and NK cells are: Fas/Fas-L, killer inhibitory receptors family (KIRs), tumor necrosis factor receptors family (TNF) and others [2-4]. Recently, a novel factor called RCAS1 has been described [4-6]. RCAS1 is a type II membrane protein, expressed in extra-villous cytotrophoblast, villi-histiocytes, uterine endometrium and in various human cancer cells [7-12]. This protein acts as a ligand for a putative receptor that may be present on normal peripheral lymphocytes such as T, B, and NK cells. RCAS1 inhibits the growth of receptor expressing cells in vitro and in vivo and induces apoptotic cell death [13]. Main functions of RCAS1 include avoiding of immune recognition and evading i