| First Author | Liu W | Year | 2013 |
| Journal | Am J Pathol | Volume | 183 |
| Issue | 2 | Pages | 441-9 |
| PubMed ID | 23746656 | Mgi Jnum | J:198725 |
| Mgi Id | MGI:5499048 | Doi | 10.1016/j.ajpath.2013.04.015 |
| Citation | Liu W, et al. (2013) Cross-Regulation of T Regulatory-Cell Response after Coxsackievirus B3 Infection by NKT and gammadelta T Cells in the Mouse. Am J Pathol 183(2):441-9 |
| abstractText | Coxsackievirus B3 (CVB3) variants H3 and H310A1 differ by a single nonconserved amino acid in the VP2 capsid region. C57Bl/6 mice infected with the H3 virus develop myocarditis correlating with activation of T cells expressing the Vgamma4 T cell receptor chain. Infecting mice with H310A1 activates natural killer T (NKT; mCD1d-tetramer(+) TCRbeta(+)) cells, but not Vgamma4 T cells, and fails to induce myocarditis. H310A1 infection preferentially activates M2 alternatively activated macrophage and CD4(+)FoxP3 (T regulatory) cells, whereas CD4(+)Th1 (IFN-gamma(+)) cells are suppressed. By contrast, H3 virus infection activates M1 proinflammatory and CD4(+)Th1 cells, but not T regulatory cells. The M1 macrophage show significantly increased CD1d expression compared to M2 macrophage. The ability of NKT cells to suppress myocarditis was shown by adoptive transfer of purified NKT cells into H3-infected NKT knockout (Jalpha18 knockout) mice, which inhibited cardiac inflammation and increased T regulatory cell response. Cardiac virus titers were equivalent in all mouse strains indicating that neither Vgamma4 nor NKT cells participate in control of virus infection. These data show that NKT and Vgamma4 cells cross-regulate T regulatory cell responses during CVB3 infections and are the primary factor determining viral pathogenesis in this mouse model. |
