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Published online before print January 10, 2007
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Vaccine and Gene Therapy Institute, Oregon Health and Science University, Beaverton, Oregon, USA
1 Correspondence: Vaccine and Gene Therapy Institute, Oregon Health and Science University, 505 N.W. 185th Avenue, Beaverton, OR 97006, USA. E-mail: slifkam{at}ohsu.edu
ABSTRACT
Previous studies have shown that T cells, which are genetically deficient in CTLA-4/CD152 expression, will proliferate uncontrollably, resulting in lethal autoimmune disease. This and other evidence indicate that CTLA-4 plays a critical role in the negative regulation of effector T cell function. In contrast to expectations, BrdU incorporation experiments demonstrated that CTLA-4 expression was associated with normal or even enhanced in vivo proliferation of virus-specific CD4+ and CD8+ T cells following acute lymphocytic choriomeningitis virus or vaccinia virus infection. When compared with CTLA-4 T cells directly ex vivo, CTLA-4+ T cells also exhibited normal antiviral effector functions following stimulation with peptide-coated cells, virus-infected cells, plate-bound anti-CD3/anti-CTLA-4, or the cytokines IL-12 and IL-18. Together, this indicates that CTLA-4 does not directly inhibit antiviral T cell expansion or T cell effector functions, at least not under the normal physiological conditions associated with either of these two acute viral infections.
Key Words: CD8 CD4 LCMV vaccinia
Related Article
J. Leukoc. Biol. 2007 81: 1176-1178.
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