| First Author | Michalek RD | Year | 2012 |
| Journal | J Virol | Volume | 86 |
| Issue | 24 | Pages | 13629-41 |
| PubMed ID | 23055551 | Mgi Jnum | J:295019 |
| Mgi Id | MGI:6459321 | Doi | 10.1128/JVI.01559-12 |
| Citation | Michalek RD, et al. (2012) Peroxiredoxin II regulates effector and secondary memory CD8+ T cell responses. J Virol 86(24):13629-41 |
| abstractText | Reactive oxygen intermediates (ROI) generated in response to receptor stimulation play an important role in cellular responses. However, the effect of increased H(2)O(2) 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. |
