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Lupus is an autoimmune disease characterized by antibodies directed against nuclear components that induce immune complex-mediated injury to multiple organs. Underlying lupus is the induction of T-cell-dependent activation and clonal expansion of autoreactive B cells in germinal centers resulting in their differentiation into plasma cells that secrete pathogenic autoantibodies. Heightened glucose metabolism is inherent to immune/inflammatory disorders, but little is known of its role in lupus etiology. Present treatments for lupus rely heavily on broad-spectrum immunosuppressive agents, and there is a need for targeted therapies that effectively counteract this systemic autoimmune disorder.

Here we examined the metabolic and gene expression profiles of key autoimmune populations in mouse models of spontaneous lupus and their responses to treatment with the glycolysis inhibitor 2 …