U. Hainz, B. Jurgens, T. Wekerle, M. G. Seidel and Andreas Heitger Pages 267 - 272 ( 6 )
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.
Indoleamine 2,3-dioxygenase, HSCT, T-cell, transplantation, tolerance, inflammation, CTLA4, GVHD
Children's Cancer Research Institute, Transplantation Immunology, Kinderspitalgasse 6, A-1090 Vienna, Austria.