Interestingly, IFNαR-/- CD4 T cells and B cells, two populations we have previously shown to be increased in IFNαR-/- mice and anti- IFNαR antibody treated mice [10], were not increased above their pre-infection levels following persistent infection of mixed bone marrow chimera mice (S2A Fig), indicating that their expansion in IFNαR-/- mice and anti- IFNαR antibody treated mice is not cell intrinsic. The gene discussed is IFNAR1; the disease is infection.