CD4 and Burkitt lymphoma: This might suggest that BL cells with latency I could evade the surveillance of EBNA-1-specific CD4 CTLs in a host with a genetic predisposition (HLA-II alleles) for developing BL, through a decrease in the activation of CD4 T cells by blocking the HLA class II/(TCR) interaction by gp42 and the release of IL-10 by decreasing the Th1 response, increasing the proliferation of Treg cells and the Th2 response.