It seems that EBV can trigger infected cells to lose expression of the iNKT cell receptor ligand CD1d and therefore makes infected cells invisible to the immune system. Restoring CD1d expression by the use of an analog of retinoic acid lead to recognition of infected cells in an experiment. Now the big question is, how we can increase CD1d expression in humans. Could we use what the scientists used? http://www.sciencedaily.com/releases/2013/10/131012093040.htm Oct. 12, 2013 — Development of a vaccine against Epstein-Barr virus (EBV) has taken a step forward with the Canadian discovery of how EBV infection evades detection by the immune system. EBV causes infectious mononucleosis and cancers such as Hodgkin's lymphoma and nasopharyngeal carcinoma, which is the most common cancer in China, as well as opportunistic cancers in people with weakened immune systems. A member of the herpes virus family that remains in the body for life, the virus infects epithelial cells in the throat and immune cells called B cells. The researchers discovered that the virus triggers molecular events that turn off key proteins, making infected cells invisible to the natural killer T (NKT) immune cells that seek and destroy EBV-infected cells. "If you can force these invisible proteins to be expressed, then you can render infected cells visible to NKT cells, and defeat the virus. This could be key to making a vaccine that would provide immunity from ever being infected with EBV," says Dr. Rusung Tan, the study's principal investigator. Dr. Tan is a scientist and director of the Immunity in Health & Disease research group at the Child & Family Research Institute at BC Children's Hospital, and a professor in the Department of Pathology at the University of British Columbia. The findings were published this week in the print edition of the scientific journal Blood. For this study, the researchers looked at cells from infected tonsils that had been removed from patients at BC Children's Hospital by Dr. Frederick Kozak. The researchers infected the tonsillar B cells with EBV, and then combined some of these cells with NKT cells. They found that more NKT cells led to fewer EBV-infected cells, while an absence of NKT cells was associated with an increase in EBV-infected cells.