PLACENTAL REGULATION OF ANTIGEN PRESENTATION.
James B. Copeman¹, Robin N.N. Han¹ and James C. Cross^1,2,3.  ¹Samuel Lunenfeld Research Institute, Mount Sinai Hospital, ²Departments of Obstetrics and Gynaecology, and ³Molecular and Medical Genetics, Univeristy of Toronto; Toronto, Ontario.


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HLA-G is a placental-specific non-classical MHC Class I molecule, which may be involved in the maternal tolerance of the semi-allogenic fetus. We are analysing the placental regulation of HLA-G and of factors involved in the loading of antigenic peptides onto Class I molecules. First trimester placentae were obtained from elective terminations of normal pregnancies. Clumps of chorionic villi were paraffin-embedded and sectioned (5um). Immunohistochemistry was performed on adjacent sections using primary antibodies to HLA-G, b2-microglobulin, TAP1, TAP2 and tapasin. Alternatively, adjacent sections were analysed by RNA in situ hybridisation, employing 33P-labelled riboprobes, specific to the aforementioned molecules. We confirmed that HLA-G and TAP1 protein expression is upregulated during the differentiation of extravillous cytotrophoblast cells (the placental cell type which invades the maternal decidua). This same expression pattern was also observed for TAP2 and tapasin. b2-microglobulin showed a similarly restricted expression pattern, although in situ hybridisation results suggested that this molecule might be upregulated earlier in extravillous cytotrophoblast differentiation than TAP1. We conclude that factors involved in peptide loading of Class I molecules might be coordinately regulated in the placenta. This expression pattern may be the mechanism for the previously-described post-transcriptional regulation of HLA-G.