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2015 ; 106
(8
): 1008-15
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Inhibition of indoleamine 2,3-dioxygenase 1 expression alters immune response in
colon tumor microenvironment in mice
#MMPMID26033215
Takamatsu M
; Hirata A
; Ohtaki H
; Hoshi M
; Ando T
; Ito H
; Hatano Y
; Tomita H
; Kuno T
; Saito K
; Seishima M
; Hara A
Cancer Sci
2015[Aug]; 106
(8
): 1008-15
PMID26033215
show ga
Indoleamine 2,3-dioxygenase (IDO), an enzyme that degrades the essential amino
acid l-tryptophan along the kynurenine pathway, exerts immunomodulatory effects
in a number of diseases. IDO expression is increased in tumor tissue and in
draining lymph nodes; this increase is thought to play a role in tumor evasion by
suppressing the immune response. A competitive inhibitor of IDO is currently
being tested in clinical trials for the treatment of relapsed or refractory solid
tumors, but the efficacy of IDO inhibition in colorectal tumors remains to be
fully elucidated. In this study, we investigated the effect of IDO deficiency on
colon tumorigenesis in mice by genetic deletion and pharmacological inhibition.
Ido1-deficient((-/-)) mice were crossed with Apc(Min/+) mice or were administered
azoxymethane with or without dextran sodium sulfate. Ido1 deficiency did not lead
to significant differences in the size and number of colon tumors. Similarly, the
pharmacological inhibition of IDO using 1-methyltryptophan (1-mT) also resulted
in no significant differences in tumor size and number in Apc(Min/+) mice.
However, Ido1 deficiency altered the immune response in the tumor
microenvironment, showing a significant increase in mRNA expression of
pro-inflammatory cytokines and a significant decrease in the number of
Foxp3-positive regulatory T cells in the colon tumors of Ido1((-/-)) mice.
Importantly, 1-mT treatment also significantly altered cytokine expression in the
colon tumor tissues. These results suggest that IDO inhibition alone cannot
sufficiently suppress colon cancer development in mice despite its
immunomodulatory activity in the tumor microenvironment.
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