Several studies including this one demonstrate an important role for IL-12 in IFN-c expression by Tconv and CD8 T cells and Tregs in vitro [5, 13] . Further, IL-12 is critical for IFN-c production by Tregs in mice with autoimmune colitis [13] . However, the requirement for IL-12 in IFN-c expression by Tconv and CD8 T cells or Tregs in virus-infected animals is less clear. To investigate whether IL-12 signaling is critical for IFN-c production by Tregs in virus-infected mice, we infected IL-12Rb2 2/2 mice with the mildly neurovirulent rJ2.2 strain of MHV [48] . We detected slightly lower frequencies of virus-specific IFN-c expressing Tregs and Tconv in IL-12Rb2 2/2 mice, consistent with a previous report showing that IL-12 modestly decreased the frequencies of virus-specific T cells in MHV-infected IL-12p35 2/2 mice [49] . The absence of IL-12 signalling may not have had a substantial effect because we detected no differences in CD25 expression on Tregs and virus-specific non-Treg T cells when cells harvested from the brains of IL-12Rb2 2/2 mice and B6 mice were compared (data not shown). Our results are also consistent with others showing IFN-c production was relatively normal in IL-12 2/2 or IL-12R 2/2 mice infected with viruses such as lymphocytic choriomeningitis virus, influenza A virus, adenovirus or hepatotropic strains of MHV. In contrast, IL-12 was essential for IFN-c expression in mice infected with some intracellular nonviral pathogens, such as Leishmania species and Toxoplasma gondii [50] .