In contrast, CD11c+T-bethi B cells were depleted in CD4cre/+ x Adora2aflox/flox mice that had been treated with CGS-21680 from days 30–37 post-infection, indicating that depletion of CD11c+T-bethi B cells did not require A2A receptor signaling on CD4+ T cells (Fig. 1e and Supplementary Fig. 3B). This evidence concerns the gene CD4 and infection.