Although the absence of CD4 and CD8 T cells epitopes in the repeat domain of TcRpL7a explains the lack of TcRpL7a-specific IFN-γ, IL-10, and antibody production in mice immunized with TcRpL7aRep, the lack of epitopes may not be the only factor responsible for the increased susceptibility to a challenging infection in animals immunized with TcRpL7aRep. Here, IFNG is linked to infection.