@article{85676,
  keywords = {Animals, Humans, Disease Models, Animal, Mice, Immune System, Mice, Transgenic, Neoplasms, Mice, Knockout, Kidney, Herpesvirus 4, Human, T-Lymphocytes, Mice, SCID, Mice, Inbred NOD, HLA-A2 Antigen, Epstein-Barr Virus Infections, Spleen},
  author = {Till Strowig and Cagan Gurer and Alexander Ploss and Yi-Fang Liu and Frida Arrey and Junji Sashihara and Gloria Koo and Charles Rice and James Young and Amy Chadburn and Jeffrey Cohen and Christian M{\"u}nz},
  title = {Priming of protective T cell responses against virus-induced tumors in mice with human immune system components.},
  abstract = {<p>Many pathogens that cause human disease infect only humans. To identify the mechanisms of immune protection against these pathogens and also to evaluate promising vaccine candidates, a small animal model would be desirable. We demonstrate that primary T cell responses in mice with reconstituted human immune system components control infection with the oncogenic and persistent Epstein-Barr virus (EBV). These cytotoxic and interferon-gamma-producing T cell responses were human leukocyte antigen (HLA) restricted and specific for EBV-derived peptides. In HLA-A2 transgenic animals and similar to human EBV carriers, T cell responses against lytic EBV antigens dominated over recognition of latent EBV antigens. T cell depletion resulted in elevated viral loads and emergence of EBV-associated lymphoproliferative disease. Both loss of CD4(+) and CD8(+) T cells abolished immune control. Therefore, this mouse model recapitulates features of symptomatic primary EBV infection and generates T cell-mediated immune control that resists oncogenic transformation.</p>
},
  year = {2009},
  journal = {J Exp Med},
  volume = {206},
  pages = {1423-34},
  month = {06/2009},
  issn = {1540-9538},
  doi = {10.1084/jem.20081720},
  language = {eng},
}