The neonatal immune system is biased to tolerogenic and Th2 type responses, compared to older children and adults. We hypothesized that one reason for altered T cell responses in early life may be active suppression by myeloid-derived suppressor cells, a heterogeneous population of activated myeloid cells with suppressive function. While a tolerant, anti-inflammatory state is likely advantageous for full-term viviparity, its persistence after birth may contribute to the reduced A 83-01 ability of infants to respond to infections and vaccinations in early life. In certain pathologies, in particular cancer and persistent inflammatory conditions, an accumulation and activation of granulocytic or monocytic MDSC that express suppressive factors such as Arginase-1, reactive oxygen species, and inducible nitric oxide synthase has been observed. The vast majority of research on MDSC to date has focused on populations of MDSC induced in murine cancer models and in humans with malignancy. Recently, high frequencies of granulocytic -MDSC were described in cord blood. In this study, we confirm these findings and further characterize the frequency and immunosuppressive function of this G-MDSC population. G-MDSC express cell markers similar to neutrophils and recently, mature neutrophils have been found to be either inflammatory or immunosuppressive. The relationship between the mature immunosuppressive neutrophils and G-MDSC has not been established, however murine transcriptomic analysis has revealed significant differences between G-MDSC and suppressive mature neutrophils. We therefore also examined the nuclear morphology and heterogeneity of the population of G-MDSC further differentiating them from mature neutrophils. Little is known about what governs the immunologic differences seen in early life, or how these change over time. An immunesuppressive feto-maternal environment appears necessary for healthy full-term gestation, as inflammation has been shown to be associated with pre-term parturition and fetal injury.Several maternal immune-suppressive mechanisms have already been identified, including regulatory T cells, regulatory NK cells, and regulatory PD-166866 (PD166866) molecule expression such as galectin-1, PDL1, and Tim3, and failure of some of these mechanisms is associated with spontaneous abortion.