In previous experiments, it has been discovered that mesenchymal stem cells (MSCs) from a lupus-prone mouse strain (Sle1a1) express a defective allele of Pbx1 (Pbx1-d), a gene that controls stemness in MSCs. Sle1a1 MSCs grow faster, differentiate quicker into osteoblasts than the B6 control, and have impaired immunosuppressive function. This data together with a significant decrease in the expression of genes associated with stemness and an increase in expression of genes associated with differentiation suggests that the Pbx1-d allele disrupts the immunoregulatory functions of MSCs. This could lead to lupus pathogenesis. We aimed to see if Pbx1-d expression in Sle1a1 MSCs increased the expression of genes promoting inflammation and activated the innate immune system. 26 genes were selected that showed an expression fold change greater than 2 in RNA sequencing as compared to B6 control MSCs. We are also investigating the metabolism of the MSCs, as cells with increased inflammatory functions display an enhanced metabolism. We are comparing the glucose metabolism and mitochondrial respiration between B6 and Sle1a1 MSC.