These predictions offer a systematic route to integrate measured information and thereby obtain testable hypotheses concerning the role of shifts in metabolic activity in SLE pathogenesis. For example, consistent with known SLE pathology, glucose consumption by TC mice is significantly higher compared to B6 mice 10 . Surprisingly, while lactate excretion by TC mice is also higher , the fraction of pyruvate excreted as lactate is similar between B6 and TC mice (67 ± 6.5% vs 65 ± 5%, Wilcoxon rank sum test 𝑝 = 0.49, 𝑛 = 4 mice for each condition). This suggests that higher lactate production by T cells of TC mice may largely be explained by their higher proliferation rate and consequent higher metabolic activity. Indeed, consistent with the model prediction, despite shifts in glucose and lactate utilization, the ratio of oxygen consumption rate (OCR) to extracellular acidification rate (ECAR), a proxy for pyruvate utilization, is similar between B6 and TC mice . In contrast, the amount of glucose entering the oxidative pentose phosphate pathway is higher in T cells from TC mice compared to B6 mice (0.017 ± 0.01 vs 0.07 ± 0.004, Wilcoxon rank sum test 𝑝 = 0.0571, 𝑛 = 4 mice for each condition). This may reflect not only the higher demand for anabolic NADPH but also the NADPH required to regenerate glutathione. While fluxes in Figure are only predictions from the computational model, these examples show that they offer numerous testable hypotheses about the utilization of nutrients.