To determine the contribution of other myeloid or lymphoid cell populations to the IFN-b production after L. monocytogenes infection, we employed tissue specific reporter mice since these mice allow tissue specific replacement of the IFN-b gene by the luciferase reporter in the IFN-b +/floxb-luc mice [30] . These mice were crossed with mice expressing Cre recombinase under various tissue specific promoters. CD19cre mice were used to implement the reporter activity in B cells, CD4cre mice in T cells and LysMcre mice in monocytes/macrophages and granulocytes. All reporter mice were heterozygous for both markers to allow normal cellular development as well as potential production of IFN-b in all cells. Comparison of such tissue specific reporter mice after Listeria infection with the ''global'' IFN-b reporter mouse (IFN-b +/Db-luc ) by whole body in vivo imaging demonstrated that T-and B-cells did not have any apparent impact on the IFN-b production after infection by L. monocytogenes (Fig. 5A) .