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2000
Volume 8, Issue 3
  • ISSN: 1389-2002
  • E-ISSN: 1875-5453

Abstract

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 mechanisms 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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/content/journals/cdm/10.2174/138920007780362554
2007-04-01
2025-10-13
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/content/journals/cdm/10.2174/138920007780362554
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  • Article Type:
    Research Article
Keyword(s): CTLA4; GVHD; HSCT; Indoleamine 2,3-dioxygenase; inflammation; T-cell; tolerance; transplantation
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