OBJECTIVES/GOALS: Preeclampsia, a hypertensive disorder in pregnancy, disrupts immune cell profiles at birth in both mice and humans. In mice, it affects offspring’s memory and behavior. This study aimed to investigate whether preeclampsia induces lasting immune cell changes after birth and its impact on astrocyte and microglia cell counts in offspring. METHODS/STUDY POPULATION: Preeclampsia was induced in C57BL/6 females by infusion of vasopressin (24 ng/hr) or saline throughout gestation via osmotic minipump. Parturition was allowed to occur naturally. Offspring were euthanized at various timepoints post-delivery for experimental measures. Total urine protein was determined via bicinchoninic acid assay. Single cell suspensions were prepared from thymus spleen, and brain tissue and separated via density gradient. Cell suspensions were stained with fluorochrome-conjugated monoclonal antibodies for flow cytometry. Statistical significance was determined using a two-tailed Student t test or one way ANOVA multiple comparisons test. The minimal level of confidence deemed statistically significant was p<0.05. RESULTS/ANTICIPATED RESULTS: Preeclampsia resulted in lower body and heart masses in offspring. Although T cell populations in the thymus were not altered in preeclampsia offspring, total T cells, Thelper, and cytotoxic T cells were elevated. Total B and isotype-switched B cells were increased in offspring of preeclampsia. Total dendritic cell percentages were not changed in offspring of preeclampsia, however, total anti-inflammatory markers on dendritic cells were reduced. Lastly, offspring of preeclampsia had a reduction in microglia and astrocytes within the brain. DISCUSSION/SIGNIFICANCE: Our study could establish including in utero data in predicting future disease risk, addressing gaps in understanding rising rates of cardiovascular and behavioral diseases. It also uncovers the impact of preeclampsia on early immune programming and reduced glial cell populations, potentially affecting cognitive and behavioral development.