Inflammatory cells of maternal origin could access the foetal villous stoma in multiple ways: The villous trophoblast barrier could be damaged. In the third trimester, syncytial knots are shed from the foetal placental villi. The shedding can strip the villous stroma. The barrier could breakdown either by upstream foetal thrombosis or ischemic damage from maternal infarction. The necrosis of syncytiotrophoblasts could arise as a result of the activation of coagulation components, complement system or platelets by antibodies or antiphospholipids. Syncytiotrophoblasts can be made to exhibit adhesion molecules (intracellular adhesion molecule 1, E-selectin) in<unk> , although in normal conditions adhesion molecules are not expressed. Maternal lymphocytes can enter the foetal stroma by passing the villous trophoblastic barrier via the anchoring villi. The anchoring villi lose their layer of continuous epithelial syncytiotrophoblast as the villi mature into invasive intermediate trophoblasts through the developmental course of the placenta. A trophic factor, IL-15, for CD8+ memory T-cells is expressed by decidual stromal cells. The trafficking of maternal lymphocytes responding to an antigen in the chronic deciduitis could activate and enter via the decidua.<unk>  is a T-cell mediated, CD8+ dominating inflammatory reaction.<unk>  develops in the foetal fibrovasculature stroma of the placenta villi usually towards the end of pregnancy (term placentas). The lymphocytes in<unk>  are of maternal origin.<unk>  is a host-derived inflammatory response happening within a donor allograft tissue. The non-T-cell component of the inflammatory infiltrate originates both from the maternal and placental side. Majority of the antigen-presenting cells were Hofbauer cells (macrophages) were of foetal origin. Perivillous monocyte-macrophages and histiocytic giant cells were of maternal origin. Foetal macrophages in<unk>  proliferate and are activated as a result of the up-regulation of MHC class 2 antigen expression. Examination of a male placenta with<unk>  demonstrated that 11.2% of the intravillous CD3+ lymphocytes were foetal, and 88.8% were maternal. Macrophages, intervillous lymphocytes, multinucleated giant cells were maternal; 10.5% of intravillous CD68+ cells and 96.4% of perivillous CD68+ cells were maternal. Lymphocytes were predominantly maternal T-cells. Maternal cells can enter the placental villi and the foetus as well.
Villitis of unknown etiology
Rhinitis medicamentosa
Mouth and genital ulcers with inflamed cartilage syndrome
Pyostomatitis vegetans
Tick-borne lymphadenopathy
Lymphedema–distichiasis syndrome
Treponematosis
Staphylococcal infection