Similarly, a previous study conducted by others [40] using T. gondii infection demonstrated that the blocking of the ICOS costimuratory pathway by an anti-B7RP-1 antibody inhibited IFN-γ production by splenocytes of infected CD28−/− mice in response to the parasite antigens in vitro, and that the treatment of CD28−/− mice with the anti-B7RP-1 antibody led to their increased mortality during the acute acquired stage of the infection. This evidence concerns the gene CD28 and infection.