| First Author | Vikingsson A | Year | 1996 |
| Journal | Cell Immunol | Volume | 173 |
| Issue | 2 | Pages | 261-8 |
| PubMed ID | 8912885 | Mgi Jnum | J:36758 |
| Mgi Id | MGI:84184 | Doi | 10.1006/cimm.1996.0276 |
| Citation | Vikingsson A, et al. (1996) Altered kinetics of CD4+ T cell proliferation and interferon-gamma production in the absence of CD8+ T lymphocytes in virus-infected beta2-microglobulin-deficient mice. Cell Immunol 173(2):261-8 |
| abstractText | CD8+ T cells are the major mediators of cytotoxic T cell activity controlling viral infections in normal mice. CD8+ T cells have also been implicated in regulating the activity of other immune cells. We have examined the possible regulatory role of CD8+ T cells on CD4+ T cells by comparing immune responses in mice expressing normal CD8+ T cell responses and in CD8+ T cell-deficient beta2-microglobulin knockout mice. In normal mice, infection with lymphocytic choriomeningitis virus (LCMV) results in a biphasic T cell immune response. First, CD8+ T cells proliferate and produce interferon-gamma (IFN-gamma), and then 2 to 4 days later CD4+ T cells proliferate and produce IFN-gamma. CD8+ T cell activity is not detected during LCMV infection in beta2-microglobulin-deficient mice. However, in beta2-microglobulin-deficient mice the CD4+ T cell expansion is exaggerated and occurs 2 days earlier than observed in normal mice. Furthermore, the CD4+ T cells have substantial cytotoxic activity, which is not observed in the CD4+ T cell population in normal mice. However, CD4+ T cell IFN-gamma production in beta2-microglobulin-deficient mice lags behind the proliferative response, resulting in a relative delay in overall T cell IFN-gamma production compared to normal mice. Taken together, these data suggest that CD8+ T cell activation peaks at an earlier time point than CD4+ T cell activation during the primary immune response to LCMV and that CD8+ T cells may inhibit CD4+ T cell proliferation and the development of CD4+ T cell cytotoxic activity. |
