No abstract

The observation that maternal cells can transfer from mother to child during pregnancy and differentiate into many different tissues including islet beta cells is exciting and intriguing, and to date has generated more questions than answers: Could these genetically distinct maternal cells play a role in the initiation of autoimmune diabetes in the child? Why do some individuals appear to have higher levels of maternal cells than others? What can we learn about how human beta cells differentiate from maternal stem cells? In this article, we review published data on maternal microchimerism in type 1 diabetes (and other autoimmune diseases) and discuss the technical limitations involved in the study of these maternally inherited cells. By improving the methodologies available for analysis of maternal cells in humans we will increasingly be in a position to answer the questions laid out above and to fully understand the biological insights generated by this experiment of nature.