Indoleamine 2,3-dioxygenase, Tregs and cancer

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

The IDO pathway is implicated in a number of settings which lead to acquired peripheral tolerance. One such setting may be the functional tolerance displayed by tumor-bearing hosts toward tumor-associated antigens. Foxp3 + Tregs are now recognized as a major contributor to tumor-induced immune suppression and functional tolerance. Emerging evidence links the IDO pathway with Treg biology at several points. The first is the ability of IDO-expressing DCs to drive the differentiation of naive CD4+ T cells toward a Foxp3+ (inducible Treg) phenotype. The second link is the ability of IDO-expressing DCs to directly activate mature, pre-existing Tregs for markedly enhanced suppression of target cells. And the third link is the ability of IDO to prevent the inflammation-induced conversion ("reprogramming") of Tregs into pro-inflammatory T-helper-like cells in vivo. Taken together, these findings suggest that IDO may represent an important regulatory checkpoint influencing Treg activity: both by stabilizing and augmenting the suppressive phenotype, and by preventing Treg reprogramming into non-suppressive helper-like cells.

Original languageEnglish (US)
Pages (from-to)2240-2246
Number of pages7
JournalCurrent Medicinal Chemistry
Volume18
Issue number15
StatePublished - May 1 2011

Fingerprint

Indoleamine-Pyrrole 2,3,-Dioxygenase
Helper-Inducer T-Lymphocytes
Tumors
Peripheral Tolerance
Phenotype
Neoplasm Antigens
Bearings (structural)
Neoplasms
T-cells
Inflammation
T-Lymphocytes
Antigens

Keywords

  • Dendritic cells
  • Foxp3
  • IDO
  • Regulatory T cells
  • Tumor immunology

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Pharmacology
  • Drug Discovery
  • Organic Chemistry

Cite this

Indoleamine 2,3-dioxygenase, Tregs and cancer. / Munn, David H.

In: Current Medicinal Chemistry, Vol. 18, No. 15, 01.05.2011, p. 2240-2246.

Research output: Contribution to journalArticle

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