Tryptophan catabolism and T cell responses

Andrew L. Mellor, David Munn, Phillip Chandler, Denn Keskin, Theodore Johnson, Brendan Marshall, Kanchan Jhaver, Babak Baban

Research output: Contribution to journalArticle

71 Scopus citations

Abstract

Cells expressing indoleamine 2,3 dioxygenase (IDO) play key roles in regulating adaptive immune responses orchestrated by T cells. In this report we discuss our working model, the tryptophan depletion hypothesis, to explain links between IDO expression and inhibition of T cell responses. We posit that IDO+ cells, particularly professional antigen presenting cells (APCs) promote T cell entry but block cell cycle progression due to tryptophan catabolism. We discuss experimental evidence supporting predictions from the tryptophan depletion hypothesis and the implications that this model has for understanding the origin of tolerant states that explain immunological paradoxes, such as fetal survival, tumor persistence and failure to eradicate pathogens like HIV that cause persistent infections.

Original languageEnglish (US)
Pages (from-to)27-35
Number of pages9
JournalAdvances in experimental medicine and biology
Volume527
StatePublished - Dec 1 2003

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ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Mellor, A. L., Munn, D., Chandler, P., Keskin, D., Johnson, T., Marshall, B., Jhaver, K., & Baban, B. (2003). Tryptophan catabolism and T cell responses. Advances in experimental medicine and biology, 527, 27-35.