Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface
Figure 1
Proposed model for antigen-presenting cells and decidual lymphocytes interactions at the maternal-foetal interface in the presence (a) and absence (b) of mucin-1- (Muc 1-) and tumour-associated glycoprotein-72 (TAG-72). The functions of dendritic cells (DCs) and macrophages (Mfgs) may be influenced by Muc 1 and TAG-72 that bind to the mannose receptor (MR) and CD209. TAG-72-shaped DCs may produce less CD83, resulting in lower proliferation and selective apoptosis of cognate cytotoxic T cells to allow survival of Th2-oriented T cells with low production of IFN-gamma (IFN-γ), attracted by CC chemokine ligand- (CCL-)19 and CCL22. Mfgs in the presence of TAG-72 produced higher levels of interleukin (IL)-10 and IL-1 receptor antagonist (IL-1RA), but significantly decreased levels of IL-12 and CCL3, support a Th2 bias. Muc 1-shaped Mfgs increased IL-1 receptor type II (IL-1R type II) expression, whereas a D6 decoy, CD80, CD86, and human leukocyte antigen (HLA)DR remain relatively unchanged. Muc 1-shaped Mfgs and TAG-72-treated DCs appear to decrease IL-15 production and cannot support the proliferation of CD56 bright NK cells and expression of cytotoxic mediators. Low IFN-γ expression by TAG-treated DCs does not support decidual vessel remodelling. During normal eutopic implantation, removing surface epithelial glycoproteins (b) allows antigen-presenting cells to support mild proinflammatory reactions by increasing IL-15 and IFN-γ production and amplifying NK cells, which are rich in cytotoxic mediators.
