A common feature in GBM is the expression of indoleamine 2,3 dioxgenase 1 (IDO), a rate-limiting enzyme that converts tryptophan (Trp) into kynurenine (Kyn). Using mouse GBM models, we have determined that, rather than the expected Trp into Kyn converting function of IDO1 resulting in suppression of the anti-GBM immune response, non-enzymatic mechanisms play a primary role. This work intends to validate these findings in human GBM and delineate the non-enzymatic mechanism(s) of IDO1-induced immune evasion in GBM.
|Effective start/end date||8/1/16 → 6/30/21|
- National Institute of Neurological Disorders and Stroke (5R01NS097851-03)
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