Abstract Pregnancy is a significant immunological event, which has been shown to induce changes in maternal T cells. Studies examining maternal T cell responses in pregnancy have largely been conducted using mice that express transgenic “surrogate” fetal antigens, and have focused mainly on divided alloreactive T cells. Yet, maternal T cells may exhibit a broader range of responses during pregnancy some of which may not rely upon TCR signaling or cellular proliferation. To investigate the full spectrum of endogenous maternal T cell responses in natural pregnancy, we used the Nur77 mouse model, which allows for a graded assessment of TCR signaling using a GFP reporter. Splenocytes from female CD45.2 Nur77 mice were labeled with CellTrace Violet (CTV) to detect cellular division and transferred into female CD45.1 congenic mice. These host females were then mated with either syngeneic CD45.1 or allogeneic Balb/c males or left naive non-mated controls. Splenocytes were collected on either embryonic day 10 or 18 (E10 or E18) and analyzed using flow cytometry. t-SNE analysis revealed few phenotypic differences between the experimental groups at E10 with significantly increased separation by E18, which was most evident in the CD4 compartment. Interestingly, this separation was driven primarily by changes in the expression of selectins (i.e. downregulation of CD62L) and cytokine receptors (i.e. increased expression of CD25) as opposed to changes in TCR signaling (GFP) or cellular division (CTV). Accordingly, we conclude that maternal T cell responses in pregnancy are significantly shaped by non-antigen driven signals. The functional impact of these non-antigen driven changes in cellular phenotype are unknown and currently under investigation.