Indoleamine 2,3-dioxygenase is a critical resistance mechanism in antitumor T cell immunotherapy targeting CTLA-4
By Rikke B. Holmgaard, D. Zamarin, D. Munn, J. Wolchok, James P. Allison. Journal of Experimental Medicine, 2013
614 citations recorded by the source corpus.
Indoleamine 2,3-dioxygenase suppresses infiltration and accumulation of tumor-reactive T cells in the context of anti–CTLA-4 immunotherapy and attenuates the anti-tumor efficacy.
Subfields: Biological Psychiatry, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/15d19cf67b87a0ad0ac0d8d6ea33fb434395cb68
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Citations in the corpus
- Immune escape mechanisms as a guide for cancer immunotherapy (2014, background): “The role of IDO as an immune resistance mechanism to immune checkpoint therapy (including anti-CTLA-4 and anti-PD-1 blocking antibodies) is supported by preclinical data (37) and is the basis for an ongoing clinical study investigating combination therapy with CTLA-4 blocking antibody ipilimumab and”
- IDO in the Tumor Microenvironment: Inflammation, Counter-regulation and Tolerance (2016, neutral): “By whatever pathway, if Akt phosphorylation on the activating Ser473 residue is blocked, then the Treg is able to maintain expression of FoxO3a and acquire a highly suppressive phenotype that includes up-regulation of cell-surface PD-1 and the lipid phosphatase PTEN.”
- Distinct Immune Cell Populations Define Response to Anti-PD-1 Monotherapy and Anti-PD-1/Anti-CTLA-4 Combined Therapy. (2019, neutral): “Multiple studies have demonstrated the importance of other immune checkpoints and proteins such as IDO1, LAG3, and TIM3 in response to immunotherapy (Holmgaard et al., 2013; Ngiow et al., 2011; Woo et al., 2012), all of which have inhibitors in drug development.”
- Resistance Mechanisms to Immune-Checkpoint Blockade in Cancer: Tumor-Intrinsic and -Extrinsic Factors. (2016, neutral): “…thecombinationof IDO inhibitors and ICB therapy has been shown to increase TILs and their functional capacities in the TME and thus mediates rejection of both IDO-expressing and -nonexpressing poorly immunogenic tumors in an experimental setting (Holmgaard et al., 2013; Spranger et al., 2014).”