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Inhibition of indoleamine 2,3-dioxygenase enhances the T-cell response to influenza virus infection.

The Journal of general virology (2013-04-13)
Julie M Fox, Leo K Sage, Lei Huang, James Barber, Kimberly D Klonowski, Andrew L Mellor, S Mark Tompkins, Ralph A Tripp
ABSTRACT

Influenza infection induces an increase in the level of indoleamine 2,3-dioxygenase (IDO) activity in the lung parenchyma. IDO is the first and rate-limiting step in the kynurenine pathway where tryptophan is reduced to kynurenine and other metabolites. The depletion of tryptophan, and production of associated metabolites, attenuates the immune response to infection. The impact of IDO on the primary immune response to influenza virus infection was determined using the IDO inhibitor 1-methyl-D,L-tryptophan (1MT). C57BL/6 mice treated with 1MT and infected with A/HKx31 influenza virus had increased numbers of activated and functional CD4⁺ T-cells, influenza-specific CD8⁺ T-cells and effector memory cells in the lung. Inhibition of IDO increased the Th1 response in CD4⁺ T-cells as well as enhanced the Th17 response. These studies show that inhibition of IDO engenders a more robust T-cell response to influenza virus, and suggests an approach for enhancing the immune response to influenza vaccination by facilitating increased influenza-specific T-cell response.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
L-Tryptophan, reagent grade, ≥98% (HPLC)
Sigma-Aldrich
L-Tryptophan, from non-animal source, meets EP, JP, USP testing specifications, suitable for cell culture, 99.0-101.0%
Sigma-Aldrich
L-Tryptophan, BioUltra, ≥99.5% (NT)
Supelco
Tryptophan, Pharmaceutical Secondary Standard; Certified Reference Material
Supelco
L-Tryptophan, certified reference material, TraceCERT®
Sigma-Aldrich
DL-Kynurenine, ≥95.0% (NT)