Patients with existing hypertension and renal disease have an increased risk for developing superimposed preeclampsia. The Dahl SS rat has been shown to be a model of superimposed spontaneous preeclampsia characterized by exacerbated hypertension, increased urinary protein excretion, and increased fetal demise. Because of the underlying immune system dysfunction present in preeclamptic pregnancies in humans, we hypothesized that the Dahl SS rat would also have an altered immune status. In the present study, Dahl SS rats fed a normal (0.3%) salt diet were compared to normal pregnant Sprague Dawley (NP) rats. On gestational day 19, spleens and placentas were collected for flow cytometric analyses. Splenic CD3 + CD4 + T cells were analyzed for cytokine production after polyclonal stimulation with phorbol myristate acetate and calcium ionophore to elicit a primary cytokine response. Dahl SS rats had increased percentages of inflammatory TNF a + T cells as compared to NP rats (4.8±0.3% vs. 1.9±0.4%, p<0.001), but there were no significant differences in percentages of IFN-γ + , IL-4 + , or IL-17 + splenic T cells. Analyses of placental lymphocytes revealed that Dahl SS rats had increased percentages of placental CD3 + CD4 + T cells as compared to NP rats (24.3±1.2% vs. 7.6±1.3% , p<0.0001) as well as CD3 + CD8 + T cells (9.2±0.5% vs. 4.9±0.4% , p<0.001), but there was no difference in CD45RA + B cells. For comparison, we also assessed placental leukocytes in the established reduced uterine perfusion pressure (RUPP) model that mimics characteristics of preeclampsia. Previous studies have reported that pregnant Sprague Dawley rats with surgically induced RUPP have aberrant immune system function which contributes to the pathophysiology of the preeclamptic phenotype in this model. While placentas from RUPP rats had an increase in placental CD3 + CD4 + T cells as compared to NP rats (14.9±1.9% vs. 7.6±1.3% p<0.001), similar to pregnant Dahl SS, the percentages of CD3 + CD8 + T cells and CD45RA + B cells were not significantly different. Taken together, these data demonstrate an association between proinflammatory T cells and superimposed preeclampsia, and suggest that different immunological mechanisms may contribute to the pathogenesis of preeclampsia in different models.