| First Author | Solomos AC | Year | 2016 |
| Journal | Virology | Volume | 499 |
| Pages | 196-202 | PubMed ID | 27677156 |
| Mgi Jnum | J:343101 | Mgi Id | MGI:7562613 |
| Doi | 10.1016/j.virol.2016.09.013 | Citation | Solomos AC, et al. (2016) CD4(+) T cells require either B cells or CD8(+) T cells to control spread and pathogenesis of a neurotropic infection. Virology 499:196-202 |
| abstractText | Immunity within the brain, specifically to virus-infected neurons, must be controlled to prevent neuron loss and impairment, though the process by which this occurs remains unclear. Here, we use a mouse model of neuron-restricted measles virus infection, in which immunocompetent adults survive challenge, whereas T and B cell-deficient mice succumb. This model allowed us to more precisely define the contributions of CD4(+) T cells, CD8(+) T cells, and B cells in neuroprotection. Both B cell knockout mice and mice depleted of CD8(+) T cells survive challenge and show no signs of illness, though are less able to control viral replication than immunocompetent mice. In contrast, depletion of CD4(+) T cells results in disease and death in all infected mice, though the kinetics of illness are delayed compared to RAG knockout mice. Our data suggest a coordinated interplay of adaptive immune components, which collectively controls viral spread and limits neuropathogenesis. |
