tetano
Editor, Senior Moderator
J Gen Virol. 2013 Apr 11. [Epub ahead of print]
Inhibition of indoleamine 2, 3- dioxygenase (IDO) enhances the T cell response to influenza virus infection.
Fox JM, Sage LK, Huang L, Barber J, Klonowski KD, Mellor AL, Tompkins M, Tripp RA.
Source
University of Georgia;
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+, 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.
PMID:
23580425
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23580425
Inhibition of indoleamine 2, 3- dioxygenase (IDO) enhances the T cell response to influenza virus infection.
Fox JM, Sage LK, Huang L, Barber J, Klonowski KD, Mellor AL, Tompkins M, Tripp RA.
Source
University of Georgia;
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+, 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.
PMID:
23580425
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/23580425