|
1
|
Fallarino F, Grohmann U, Vacca C, et al: T
cell apoptosis by tryptophan catabolism. Cell Death Differ.
9:1069–1077. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
2
|
Fallarino F, Grohmann U, You S, et al: The
combined effects of tryptophan starvation and tryptophan
catabolites down-regulate T cell receptor zeta-chain and induce a
regulatory phenotype in naive T cells. J Immunol. 176:6752–6761.
2006. View Article : Google Scholar : PubMed/NCBI
|
|
3
|
Frumento G, Rotondo R, Tonetti M, Damonte
G, Benatti U and Ferrara GB: Tryptophan-derived catabolites are
responsible for inhibition of T and natural killer cell
proliferation induced by indoleamine 2,3-dioxygenase. J Exp Med.
196:459–468. 2002. View Article : Google Scholar : PubMed/NCBI
|
|
4
|
Munn DH, Zhou M, Attwood JT, et al:
Prevention of allogeneic fetal rejection by tryptophan catabolism.
Science. 281:1191–1193. 1998. View Article : Google Scholar : PubMed/NCBI
|
|
5
|
Mellor AL, Sivakumar J, Chandler P, et al:
Prevention of T cell-driven complement activation and inflammation
by tryptophan catabolism during pregnancy. Nat Immunol. 2:64–68.
2001. View Article : Google Scholar : PubMed/NCBI
|
|
6
|
Mellor AL and Munn DH: IDO expression by
dendritic cells: tolerance and tryptophan catabolism. Nat Rev
Immunol. 4:762–774. 2004. View
Article : Google Scholar : PubMed/NCBI
|
|
7
|
Inaba T, Ino K, Kajiyama H, et al: Role of
the immunosuppressive enzyme indoleamine 2,3-dioxygenase in the
progression of ovarian carcinoma. Gynecol Oncol. 115:185–192. 2009.
View Article : Google Scholar : PubMed/NCBI
|
|
8
|
Ino K, Yamamoto E, Shibata K, et al:
Inverse correlation between tumoral indoleamine 2,3-dioxygenase
expression and tumor-infiltrating lymphocytes in endometrial
cancer: its association with disease progression and survival. Clin
Cancer Res. 14:2310–2317. 2008. View Article : Google Scholar : PubMed/NCBI
|
|
9
|
Sharma MD, Baban B, Chandler P, et al:
Plasmacytoid dendritic cells from mouse tumor-draining lymph nodes
directly activate mature Tregs via indoleamine 2,3-dioxygenase. J
Clin Invest. 117:2570–2582. 2007. View
Article : Google Scholar : PubMed/NCBI
|
|
10
|
Platten M, Ho PP, Youssef S, et al:
Treatment of autoimmune neuroinflammation with a synthetic
tryptophan metabolite. Science. 310:850–855. 2005. View Article : Google Scholar : PubMed/NCBI
|
|
11
|
Jasperson LK, Bucher C,
Panoskaltsis-Mortari A, et al: Indoleamine 2,3-dioxygenase is a
critical regulator of acute graft-versus-host disease lethality.
Blood. 111:3257–3265. 2008. View Article : Google Scholar
|
|
12
|
Jasperson LK, Bucher C,
Panoskaltsis-Mortari A, Mellor AL, Munn DH and Blazar BR: Inducing
the tryptophan catabolic pathway, indoleamine 2,3-dioxygenase
(IDO), for suppression of graft-versus-host disease (GVHD)
lethality. Blood. 114:5062–5070. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
13
|
Gupta S, Barrett T, Whitmarsh AJ, et al:
Selective interaction of JNK protein kinase isoforms with
transcription factors. EMBO J. 15:2760–2770. 1996.PubMed/NCBI
|
|
14
|
Hu D and Kipps T: Reduction in
mitochondrial membrane potential is an early event in
Fas-independent CTL-mediated apoptosis. Cell Immunol. 195:43–52.
1999. View Article : Google Scholar : PubMed/NCBI
|
|
15
|
Tohda S, Nara N, Murohashi I and Aoki N:
Establishment of an interleukin-3-dependent leukemic cell line from
a patient with chronic lymphocytic leukemia in the acute phase.
Blood. 78:1789–1794. 1991.PubMed/NCBI
|
|
16
|
Opitz CA, Litzenburger UM, Sahm F, et al:
An endogenous tumour-promoting ligand of the human aryl hydrocarbon
receptor. Nature. 478:197–203. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
17
|
Nguyen NT, Kimura A, Nakahama T, et al:
Aryl hydrocarbon receptor negatively regulates dendritic cell
immunogenicity via a kynurenine-dependent mechanism. Proc Natl Acad
Sci USA. 107:19961–19966. 2010. View Article : Google Scholar : PubMed/NCBI
|
|
18
|
Prud’homme GJ, Glinka Y, Toulina A, Ace O,
Subramaniam V and Jothy S: Breast cancer stem-like cells are
inhibited by a non-toxic aryl hydrocarbon receptor agonist. PLoS
One. 5:e138312010. View Article : Google Scholar
|
|
19
|
Maby-El Hajjami H, Amé-Thomas P, Pangault
C, et al: Functional alteration of the lymphoma stromal cell niche
by the cytokine context: role of indoleamine-2,3 dioxygenase.
Cancer Res. 69:3228–3237. 2009. View Article : Google Scholar : PubMed/NCBI
|
|
20
|
Godin-Ethier J, Hanafi LA, Duvignaud JB,
Leclerc D and Lapointe R: IDO expression by human B lymphocytes in
response to T lymphocyte stimuli and TLR engagement is biologically
inactive. Mol Immunol. 49:253–259. 2011. View Article : Google Scholar : PubMed/NCBI
|
|
21
|
Ninomiya S, Hara T, Tsurumi H, et al:
Indoleamine 2,3-dioxy-genase in tumor tissue indicates prognosis in
patients with diffuse large B-cell lymphoma treated with R-CHOP.
Ann Hematol. 90:409–416. 2011. View Article : Google Scholar
|
|
22
|
Rogosnitzky M, Danks R and Kardash E:
Therapeutic potential of tranilast, an anti-allergy drug, in
proliferative disorders. Anticancer Res. 32:2471–2478.
2012.PubMed/NCBI
|
|
23
|
Platten M, Eitel K, Wischhusen J, Dichgans
J and Weller M: Involvement of protein kinase Cdelta and
extracellular signal-regulated kinase-2 in the suppression of
microglial inducible nitric oxide synthase expression by
N-[3,4-dimethoxycinnamoyl]-anthranilic acid (tranilast). Biochem
Pharmacol. 66:1263–1270. 2003. View Article : Google Scholar : PubMed/NCBI
|
|
24
|
Chikaraishi A, Hirahashi J, Takase O, et
al: Tranilast inhibits interleukin-1beta-induced monocyte
chemoattractant protein-1 expression in rat mesangial cells. Eur J
Pharmacol. 427:151–158. 2001. View Article : Google Scholar : PubMed/NCBI
|
|
25
|
Johnson GL and Nakamura K: The c-jun
kinase/stress-activated pathway: regulation, function and role in
human disease. Biochim Biophys Acta. 1773:1341–1348. 2007.
View Article : Google Scholar : PubMed/NCBI
|
|
26
|
Behrens A, Sibilia M and Wagner EF:
Amino-terminal phosphorylation of c-Jun regulates stress-induced
apoptosis and cellular proliferation. Nat Genet. 21:326–329. 1999.
View Article : Google Scholar : PubMed/NCBI
|
