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Tumoral Immune Resistance Mediated by Enzymes That Degrade Tryptophan

Nicolas van Baren1, Benoît J Van den Eynde2

  • 1Ludwig Institute for Cancer Research, Brussels, Belgium. de Duve Institute, Université catholique de Louvain, Brussels, Belgium.

Cancer Immunology Research
|August 14, 2015
PubMed

Insights

Tumors resist T-lymphocyte attacks by degrading tryptophan. Blocking tryptophan-degrading enzymes like indoleamine 2,3-dioxygenase 1 (IDO1) can restore anti-tumor immunity, offering a therapeutic strategy.

Area of Science:

  • Cancer Immunology
  • Tumor Microenvironment
  • Immunometabolism

Background:

  • Tumors evade T-lymphocyte responses through various resistance mechanisms.
  • Tryptophan catabolism by tumor cells is a significant mechanism of immune evasion.
  • Tryptophan-degrading enzymes are frequently expressed in human tumors, inhibiting T-cell function.

Purpose of the Study:

  • To discuss the role of key enzymes in tryptophan catabolism and their impact on tumoral immune resistance.
  • To highlight the potential of pharmacologic inhibitors in restoring T-cell-mediated tumor cell killing.
  • To address discrepancies between human and mouse data regarding these enzymes.

Main Methods:

  • Review of existing literature on tryptophan catabolism and cancer immunology.
  • Analysis of data concerning indoleamine 2,3-dioxygenase 1 (IDO1), tryptophan 2,3-dioxygenase (TDO), and indoleamine 2,3-dioxygenase 2 (IDO2).
  • Comparison of findings from human and mouse studies.

Main Results:

  • Tryptophan catabolism by specific enzymes is a critical factor in tumor immune resistance.
  • Pharmacologic inhibition of these enzymes shows promise in restoring anti-tumor immune responses.
  • Differences in enzyme roles and expression exist between human and mouse models.

Conclusions:

  • Targeting tryptophan-degrading enzymes represents a promising therapeutic strategy in cancer immunotherapy.
  • Further research is needed to fully elucidate the distinct roles of IDO1, TDO, and IDO2 in different cancer contexts.
  • Understanding species-specific differences is crucial for effective clinical translation.

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