| First Author | Preiss NK | Year | 2020 |
| Journal | J Immunol | Volume | 205 |
| Issue | 12 | Pages | 3372-3382 |
| PubMed ID | 33188072 | Mgi Jnum | J:300377 |
| Mgi Id | MGI:6502547 | Doi | 10.4049/jimmunol.2000734 |
| Citation | Preiss NK, et al. (2020) Control of B Cell Lymphoma by Gammaherpesvirus-Induced Memory CD8 T Cells. J Immunol 205(12):3372-3382 |
| abstractText | Persistent infection with gammaherpesviruses (gammaHV) can cause lymphomagenesis in immunocompromised patients. Murine gammaHV-68 (MHV-68) is an important tool for understanding immune factors contributing to gammaHV control; however, modeling control of gammaHV-associated lymphomagenesis has been challenging. Current model systems require very long incubation times or severe immune suppression, and tumor penetrance is low. In this report, we describe the generation of a B cell lymphoma on the C57BL/6 background, which is driven by the Myc oncogene and expresses an immunodominant CD8 T cell epitope from MHV-68. We determined MHV-68-specific CD8 T cells in latently infected mice use either IFN-gamma or perforin/granzyme to control gammaHV-associated lymphoma, but perforin/granzyme is a more potent effector mechanism for lymphoma control than IFN-gamma. Consistent with previous reports, CD4-depleted mice lost control of virus replication in persistently infected mice. However, control of lymphoma remained intact in the absence of CD4 T cells. Collectively, these data show the mechanisms of T cell control of B cell lymphoma in gammaHV-infected mice overlap with those necessary for control of virus replication, but there are also important differences. This study establishes a tool for further dissecting immune surveillance against, and optimizing adoptive T cell therapies for, gammaHV-associated lymphomas. |
