Along with the allogeneic foetus tolerance at the maternal interface is there some remanence of this mechanism that renders the mother less reactive when receiving a graft of father cells?
As in tolerance to self, multiple mechanisms are working here: 1) The absence of classical MHC class I and II molecules on trophoblast and placenta cells; 2) The presence of HLA-G (ligand for inhibitory receptors of CTL and NK cells) on placenta cells; 3) The absence of MHC class II positive DC in placenta; 4) Expression of FasL on placenta cells; 5) Progesterone induces immune deviation to Th2 and regulatory responses with production of antiinflammatory cytokines (Il-4, IL-10 and TGFbeta2); 6) DAF and MCP prevent complement activation; 7) IDO suppresses T cell activation. Finally, I would add classical phenomenon known as "enhancement effect" of antibodies after transplantation, when maternal antibodies shade fetus from the recognition by CTLs.
Yes! Allo-TCR transgenic mice reduce the density of TCRs on T cells if foetus expresses corresponding parental MHC. Moreover, allogeneic tumors can grow in these pregnant mice. After the birth the density of TCRs is restored and allogeneic tumor is rejected. This example is described in Janeway's Immunobiology.