| First Author | Raué HP | Year | 2007 |
| Journal | J Leukoc Biol | Volume | 81 |
| Issue | 5 | Pages | 1165-75 |
| PubMed ID | 17215523 | Mgi Jnum | J:121853 |
| Mgi Id | MGI:3712403 | Doi | 10.1189/jlb.0806535 |
| Citation | Raue HP, et al. (2007) Pivotal advance: CTLA-4+ T cells exhibit normal antiviral functions during acute viral infection. J Leukoc Biol 81(5):1165-75 |
| abstractText | 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. |
