Upon EBV infection, the inventors found that IL-27 is produced by infected B lymphocytes and IL27RAIL-27 interaction is required for
in vitro maintenance and expansion of EBV-transformed B cells, potentially explaining the favorable outcome of the EBV
viral disease in IL27RA-deficient patients. In addition, the inventors identified neutralizing anti-IL27 autoantibodies in individuals who developed sporadic infectious
mononucleosis, thus possibly phenocopying the IL27RA deficiency. Collectively, these results demonstrate the critical role of IL27-IL27RA axis in
immunity to EBV, but also the hijacking of this defense by EBV to promote expansion of infected cells. The IL27-IL27RA could therefore represent a novel therapeutic target to inhibit EBV-driven B lymphoproliferative diseases.