Peroxiredoxin II regulates effector and secondary memory CD8+ T cell responses

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Title
Peroxiredoxin II regulates effector and secondary memory CD8+ T cell responses
Author(s)
R D Michalek; K E Crump; A E Weant; E M Hiltbold; D G Juneau; E Y Moon; Dae Yeul Yu; L B Poole; J M Grayson
Bibliographic Citation
Journal of Virology, vol. 86, no. 24, pp. 13629-13641
Publication Year
2012
Abstract
Reactive oxygen intermediates (ROI) generated in response to receptor stimulation play an important role in cellular responses. However, the effect of increased H2O2 on an antigen-specific CD8+ T cell response was unknown. Following T cell receptor (TCR) stimulation, the expression and oxidation of peroxiredoxin II (PrdxII), a critical antioxidant enzyme, increased in CD8+ T cells. Deletion of PrdxII increased ROI, S phase entry, division, and death during in vitro division. During primary acute viral and bacterial infection, the number of effector CD8+ T cells in PrdxII-deficient mice was increased, while the number of memory cells were similar to those of the wild-type cells. Adoptive transfer of P14 TCR transgenic cells demonstrated that the increased expansion of effector cells was T cell autonomous. After rechallenge, effector CD8+ T cells in mutant animals were more skewed to memory phenotype than cells from wild-type mice, resulting in a larger secondary memory CD8+ T cell pool. During chronic viral infection, increased antigen-specific CD8+ T cells accumulated in the spleens of PrdxII mutant mice, causing mortality. These results demonstrate that PrdxII controls effector CD8+ T cell expansion, secondary memory generation, and immunopathology.
ISSN
0022-538X
Publisher
Amer Soc Microb
DOI
http://dx.doi.org/10.1128/JVI.01559-12
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
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