Changes in expression of the<scp>CD</scp>200 tolerance‐signaling molecule and its receptor (<scp>CD</scp>200R) by villus trophoblasts during first trimester missed abortion and in chronic histiocytic intervillositis

ProblemExpression ofCD200 at the feto‐maternal interface is associated with successful murine and human pregnancy.CD200 binding toCD200 receptors on lymphomyeloid cells suppresses inflammation and induces Tregs.CD200 receptors are also expressed on mouse and human placental trophoblast cells. What is the expression ofCD200 andCD200R in human missed abortions which have preserved Treg levels and in chronic histiocytic intervillositis (CHI) where maternal inflammatory cells causeIUGR?MethodsImmunohistiochemistry forCD200,CD200R, and Ki67 using human placental sections from missed abortions, term placenta, andCHI.PCRtesting was done for trisomy in missed abortion.ResultsCD200 andCD200R were expressed by human villus trophoblasts from 2 weeks post‐implantation to term. Cytotrophoblast proliferation (Ki‐67+count) decreased at term. In first trimester missed abortion cases,CD200>CD200R villus trophoblasts accompanied missed abortion of non‐trisomic male fetuses.CD200 and Ki67+trophoblast proliferation was preserved inCHIwith maternal inflammatory cell infiltration butCD200R was greatly decreased.ConclusionResidualCD200 activity may prevent completion of abortions via induction of Treg cells. InCHI, infiltrating maternal effector T cells may block Treg induction. An autocrine role forCD200‐CD200R interaction versus inhibition of solubleCD200 by solubleCD200R is discussed.