Abstract
OBJECTIVE Glioblastoma (GBM) patients with high intratumoral IDO1 mRNA levels have an associated decrease in survival (Zhai et al., 2017; CCR). IDO1 is an immunosuppressive mediator that metabolizes tryptophan (Trp), and through its associated enzyme activity, has long been recognized to increase immunosuppressive CD4+CD25+FoxP3+ Tregs. Accordingly, we previously showed that the genetic knockdown of IDO1 in murine glioma cells, suppresses intratumoral Treg recruitment and increases animal subject survival. Unexpectedly, however, IDO1 knockdown has no effect on intratumoral Trp metabolism (Zhai et al., 2017; BBI). Further surprisingly, we recently demonstrated that, although IDO1 overexpression increases Treg levels in brain tumors, the pharmacological inhibition of IDO1 metabolism has no effect on Treg accumulation (Ladomersky et al., 2018; CCR). These novel data led us to question the requirement for IDO1 enzyme activity to regulate Tregs in malignant glioma.
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