Over the last half century, many attempts to explain the survival of the semiallogenic fetal graft have been proposed. One of the earliest explanations was based on the theory of antigenic immaturity of the embryo-fetus. This was disproved by Billingham (1964) who showed that transplantation (HLA) antigens are demonstrable very early in embryonic life. The trophoblasts are the only cells of the conceptus in direct contact with maternal tissues or blood and these tissues are genetically identical with fetal tissues. Another explanation was based on diminished immunological responsiveness of the pregnant woman. There is, however, no evidence for this to be other than an ancillary factor. In a third explanation, the uterus (decidua) is proposed as an immunologically privileged tissue site. Clearly, transplantation immunity can be evoked and expressed in the uterus as in other tissues. Therefore, the acceptance and the survival of the conceptus in the maternal uterus must be attributed to an immunological peculiarity of the trophoblasts, not the decidua.
[...] Before blastocyst implantation in the mouse, MHC class I antigens on the trophectoderm are expressed in low levels, but these antigens disappear at the time of implantation, not to reappear except later in selected subpopulations of trophoblasts in the mature placenta. TROPHOBLAST HLA CLASS I EXPRESSION. King and Loke (1991) reasoned that normal implantation is dependent upon controlled trophoblastic invasion of maternal endometrium/decidua and the spiral arteries—a mechanism for permitting and then limiting trophoblast invasion. They suggested that such a system involves the uterine large granular lymphocytes (LGLs) and the unique expression (or absence thereof) of a specific monomeric HLA class I gene in trophoblasts. [...]
[...] As described by Feinberg and colleagues (1991), oncofetal fibronectin (onfFN) molecules are characterized by a unique glycopeptide of the fibronectin molecule. They refer to onfFN as trophouteronectin or trophoblast glue to suggest a critical role for this protein in the migration and attachment of trophoblasts to maternal decidua. They localized onfFN to the junction of cytotrophoblast with extracellular matrix. Importantly, onfFN was localized to the extracellular matrix connecting extravillous cytotrophoblasts and cytotrophoblastic cell columns to the uterine decidua. As onfFN is formed by extravillous trophoblasts, including those of the chorion laeve, these investigators suggest that it may function to facilitate separation of the extraembryonic tissues from the uterus at delivery. [...]
[...] They are present in large numbers only at the midluteal phase of the cycle—at the expected time of implantation (Johnson and colleagues, 1999). These LGLs1 have a distinct phenotype characterized by a high surface density of CD56 or neural cell adhesion molecule (Loke and King, 1995). Near the end of the luteal phase of nonfertile ovulatory cycles, the nuclei of the uterine LGLs1 begin to disintegrate. With blastocyst implantation, these cells persist in the decidua during the early weeks of pregnancy. [...]
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