Partial otubain 1 deficiency compromises fetal well-being in allogeneic pregnancies despite no major changes in the dendritic cell and T cell compartment.

objectivePregnancy is characterized by well-defined immunological adaptions within the maternal immune cell compartment allowing the survival of a genetically disparate individual in the maternal womb. Phenotype and function of immune cells are largely determined by intracellular processing of external stimuli. Ubiquitinating and deubiquitinating enzymes are known to critically regulate immune signaling either by modulating the stability or the interaction of the signaling molecules. Accordingly, if absent, critical physiological processes may be perturbed such as fetal tolerance induction. Based on previous findings that mice hemizygous for the deubiquitinating enzyme otubain 1 (OTUB1) do not give rise to homozygous progeny, here, we investigated whether partial OTUB1 deficiency influences fetal-wellbeing in a syngeneic or an allogeneic pregnancy context accompanied by changes in the dendritic cell (DC) and T cell compartment.

resultsWe observed increased fetal rejection rates in allogeneic pregnant OTUB1 heterozygous dams but not syngeneic pregnant OTUB1 heterozygous dams when compared to OTUB1 wildtype dams. Fetal demise in allogeneic pregnancies was not associated with major changes in maternal peripheral and local DC and T cell frequencies. Thus, our results suggest that OTUB1 confers fetal protection, however, this phenotype is independent of immune responses involving DC and T cells.