Placental cd95 ligand expression is not required for fetal viability in allogeneic pregnancy

Amy Malecki Rogers, John H. Russell

Research output: Contribution to journalArticlepeer-review

Abstract

Immunologie mechanisms of maternal acceptance of a semi allogeneic fetus during pregnancy are being studied. It was hypothesized that in the placenta, which forms the site of most intimate contact between maternal and fetal tissues, expression of fas ligand (CD95L) could eliminate maternal T cells reactive against fetal antigens. CD95L is a type II transmembrane protein of the TNF family which is able to induce apoptotic death of activated T lymphocytes which express its receptor, fas (CD95). This CD95-mediated activation-induced death is important for downregulating peripheral immune responses, thereby avoiding excessive lymphoproliferation and autoimmunity. 14 day murine placentas were harvested, and cell populations separated over Percoll gradients. Cell fractions were tested for CD95L mRNA expression by reverse transcription-PCR. A trophoblast-enriched cell fraction was found to be positive. Fetal origin of the CD95L message in this fraction was confirmed by mating with a gld/gld mutant male, which carries a point mutation in the CD95L gene that can be detected in an optimized PCR assay. Breeding experiments were performed to test whether CD95L expression by placenta is important in vivo . BALB/c females (H2d) heterozygous at the gld locus (gld /+) were mated to homozygous mutant C3H.g/d males (H1k). If placenta! CD95L expression contributes significantly to fetal viability, then a deviation from the predicted ratio of 50% gld /+, 50% gld/gld progeny would be expected, favoring survival of the hétérozygotes. In fact, the Mendelian distribution was observed among offspring of these crosses even after the mothers were primed by intraperitoneal injection of paternal splenocytes.

Original languageEnglish
Pages (from-to)A1364
JournalFASEB Journal
Volume10
Issue number6
StatePublished - Dec 1 1996

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