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Peroxiredoxin II Regulates CD8+ T Cell Expansion and Survival During Acute and Chronic Viral Infections
Author(s) -
Michalek Ryan D,
Weant Ashley E,
Moon EunYi,
Yu DaeYeul,
Grayson Jason M
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.663.21
Subject(s) - cd8 , biology , clone (java method) , t cell , peroxiredoxin , cytotoxic t cell , immune system , t cell receptor , effector , microbiology and biotechnology , immunology , in vitro , enzyme , biochemistry , dna , peroxidase
Reactive oxygen intermediates (ROI) generated in response to receptor stimulation play an important role in cellular responses. We examined the role of the antioxidant enzyme, Peroxiredoxin II (PrxII), during T cell activation and throughout the immune response to acute and chronic viral infections. Following TCR stimulation, PrxII levels increased 50‐fold by 30 hours. Examination of differentiated T cells demonstrated that effector cells possessed lower PrxII levels than naïve or memory CD8 + T cells. Utilizing mice deficient in PrxII, we determined that ROI levels measured in T cells, either directly ex vivo or in response to stimulation, were higher than wild‐type mice. Deletion of PrxII also increased in vitro T cell proliferation, but decreased cell survival during division. Acute infection of PrxII −/− mice with LCMV Armstrong revealed an increased expansion of effector CD8 + T cells on day 8, but yielded no significant difference in memory CD8 + T cells by day 97. Additionally, no differences were observed in virus‐specific CD4 + T cells or antibody secreting cells at any time during infection. In contrast, chronic infection with LCMV Clone 13 resulted in death by day 13 post infection. Together, these results demonstrate that redox regulation of T cell activation through PrxII is critical during acute and chronic viral infections. Supported by ACS‐ #RSG‐04‐066‐01‐MBC to J.G.