Liu YH et al. Amniotic epithelial cells from the human placenta potently suppress a mouse model of multiple sclerosis. PLoS One. 2012;7(4):e35758. Epub 2012 Apr 26
Human amniotic epithelial cells (hAEC) have stem cell-like features and immunomodulatory properties. Here we show that hAEC significantly suppressed splenocyte proliferation in vitro and potently attenuated a mouse model of multiple sclerosis (MS). Central nervous system (CNS) CD3(+) T cell and F4/80(+) monocyte/macrophage infiltration and demyelination were significantly reduced with hAEC treatment. Besides the known secretion of prostaglandin E2 (PGE2), we report the novel finding that hAEC utilize transforming growth factor-β (TGF-β) for immunosuppression. Neutralization of TGF-β or PGE2 in splenocyte proliferation assays significantly reduced hAEC-induced suppression. Splenocytes from hAEC-treated mice showed a Th2 cytokine shift with significantly elevated IL-5 production. While transferred CFSE-labeled hAEC could be detected in the lung, none were identified in the CNS or in lymphoid organs. This is the first report documenting the therapeutic effect of hAEC in a MS-like model and suggest that hAEC may have potential for use as therapy for MS.
This study shows the effect of injecting human stem cell-like cells from the placenta, into a mouse that were induced to develop MS-like disease. As can be seen above, the cells appeared to inhibit the development of disease, the control got nothing (should have been dead human cells) whereas the test group got the human cells (hAEC). The majority of animals did not have disease when the cells were first administered the vast majority of animals then went onto have disease. Is this potent? This effect would be similar or worse with many standard immunosuppressive agents in such models.
All the things about the histology CD3, F4/80, myelin infiltrate followed what was seen neurologically and then the mechanism was reported to be a Th2 shift. although transforming growth factor (TGF) was reported to be the mechanism of disease control. Following the transfer the cells could not be found and so they have no stem cell capapbilities to transform into nerve cells, oligodendrocytes, because they are of human origin they were probably rejected by the mouse immune system, within a few (maybe 4-6 days). A few years ago we could get similar results with mouse fibroblasts that produced TGF. However this approach could be taylor made for a fad treatment, as a few years ago umbilllcal cord stem cells were peddled as a cure for MS.