Journal
CURRENT DRUG METABOLISM
Volume 8, Issue 3, Pages 267-272Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138920007780362554
Keywords
indoleamine 2,3-dioxygenase; HSCT; T-cell; transplantation; tolerance; inflammation; CTLA4; GVHD
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Hematopoietic stem cell transplantation (HSCT) is complicated by unwelcome side-effects that arise on the basis of an altered immune system. Infectious complications and alloreactive T-cell responses trigger a process of ongoing immune activation and inflammation. Negative-feedback rnechanisms to counteract inflammation involve the induction of the immunoregulatory enzyme indoleamine 2,3-dioxygenase (IDO), which mediates anti-inflammatory activities and T-cell inhibition via tryptophan catabolism. However, persistent immune activation and generalized release of pro-inflammatory cytokines deviate immune regulation towards chronic suppression incapable to abrogate the inflammatory response. This review focuses on the unique role of tryptophan catabolism in modulating inflammatory processes and T-cell responses after HSCT.
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