Indoleamine 2,3-dioxygenase in cancer: targeting pathological immune tolerance with small-molecule inhibitors

被引:87
作者
Muller, AJ [1 ]
Malachowski, WP [1 ]
Prendergast, GC [1 ]
机构
[1] Lankenau Inst Med Res, Wynnewood, PA 19096 USA
关键词
1-methyl-tryptophan (1MT); antigen-presenting cell (APC); Bin; 1; chemotherapy; dendritic cell (DC); Indo; indoleamine 2,3-dioxygenanse (IDO); macrophage; tryptophan; tumour;
D O I
10.1517/14728222.9.4.831
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Indoleamine 2,3-dioxygenase (IDO) is an interferon (IFN)-gamma-inducible, extrahepatic enzyme that catalyses the initial and rate-limiting step in the degradation of the essential amino acid tryptophan. Elevated tryptophan catabolism mediated by IDO is associated with a wide variety of human cancers and has historically been thought to be a tumoricidal consequence of IFN-gamma exposure. Evidence of a physiological requirement for IDO activity in protecting the allogeneic fetus from rejection by the maternal immune system has stimulated a radical shift in thinking about the role of IDO in cancer. Evidence now suggests that tumours can exploit IDO-mediated peripheral tolerance to promote immune escape. This review summarises key studies that implicate IDO as an important mediator of peripheral immune tolerance as well as the development of a promising new anticancer modality that incorporates the use of IDO inhibitors. The second part focuses on the current state of development of IDO inhibitory compounds as potential pharmaceutical agents.
引用
收藏
页码:831 / 849
页数:19
相关论文
共 145 条
[1]   Tuning tumor-specific T-cell activation: a matter of costimulation? [J].
Abken, H ;
Hombach, A ;
Heuser, C ;
Kronfeld, K ;
Seliger, B .
TRENDS IN IMMUNOLOGY, 2002, 23 (05) :240-245
[2]  
Aboagye-Mathiesen G, 1999, ELECTROPHORESIS, V20, P344, DOI 10.1002/(SICI)1522-2683(19990201)20:2<344::AID-ELPS344>3.0.CO
[3]  
2-V
[4]  
AMBANELLI U, 1962, Haematol Lat, V5, P49
[5]  
[Anonymous], 1994, MED CHEM RES
[6]  
AWWAD M, 1988, IMMUNOLOGY, V65, P87
[7]   Immunomodulating anticancer alkylating drugs: Targets and mechanisms of activity [J].
Ben-Efraim, S .
CURRENT DRUG TARGETS, 2001, 2 (02) :197-212
[8]   THE PREFERRED ROUTE OF KYNURENINE METABOLISM IN THE RAT [J].
BENDER, DA ;
MCCREANOR, GM .
BIOCHIMICA ET BIOPHYSICA ACTA, 1982, 717 (01) :56-60
[9]   METABOLISM OF TRYPTOPHAN .2. METABOLISM OF TRYPTOPHAN IN PATIENTS SUFFERING FROM CANCER OF THE BLADDER [J].
BOYLAND, E ;
WILLIAMS, DC .
BIOCHEMICAL JOURNAL, 1956, 64 (03) :578-582
[10]   URINARY AND BRAIN BETA-CARBOLINE-3-CARBOXYLATES AS POTENT INHIBITORS OF BRAIN BENZODIAZEPINE RECEPTORS [J].
BRAESTRUP, C ;
NIELSEN, M ;
OLSEN, CE .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1980, 77 (04) :2288-2292