Research Interests

Maternal / fetal immune interactions

During pregnancy, the foreign antigens of the fetus and placenta come into direct contact with cells of the maternal immune system but fail to evoke the typical tissue rejection response seen with surgical organ transplants. My laboratory is interested in the cellular and molecular basis of this immunological paradox. Much of our work focuses on the unique immune properties of the maternal decidua, the specialized endometrial stromal tissue that forms in response towards the implanting embryo to ultimately form a shell around the developing fetus and placenta. Despite its importance for embryogenesis, the development and function of the decidua remains very poorly understood. On the one hand, we are pursuing the possibility that decidual tissue impairs the overall function of dendritic cells. These cells are the most potent antigen presenting cells in the body and are critical for initiating T cell-mediated immune responses within lymph nodes. In particular, we are interested in whether chemokine gradients within the decidua are able to direct dendritic cell chemotaxis towards lymphatic vessels and thus allow dendritic cells at the maternal/fetal interface to migrate to the draining lymph nodes. Additionally, we are pursuing the possibility that decidual tissue inhibits the local accumulation of activated and potentially embryotoxic T cells. This might occur through altered expression of adhesion molecules or extracellular matrix factors that decrease T cell homing, or through altered expression of stromal cell-derived survival or death factors that locally increase rates of T cell death. Our work lies at the intersection of development biology and immunology and dramatically highlights how developmental events in a peripheral tissue (i.e. the differentiation of the uterine endometrium into the decidua) can influence the overall outcome of a local immune response. We believe that understanding the basis of decidual immune “privilege” will give us immune response. For example, changes in the properties of stromal tissue may be exploited by pathogens or by tumor cells to avoid immunological attack, or might be involved in the pathogenesis of autoimmunity. Understanding how stromal tissue regulates immune responses may also ultimately lead to new ways to inhibit graft rejection.