During Listeria monocytogenes infection, IFN-b is produced in spleen and lymph nodes Different strains of Listeria monocytogenes vary in their ability to activate type I IFN production [31] . Here we compared LO28 and EGDe, two commonly used strains of Listeria monocytogenes. First, we asked when and where type I IFN is induced. To address this question, we used a previously described IFN-b reporter mouse, which allows whole body in vivo imaging of IFN-b induction using firefly luciferase as a reporter [30] . Figure 1A shows induction of IFN-b in albino IFN-b +/Db-luc reporter mice after intravenous (i.v.) injection of Listeria monocytogenes LO28 and EGDe strains. At 24 hours post infection (p.i.), IFN-b induction occurred almost exclusively in the spleen. Interestingly, 48 hours p.i. a bright luminescent signal appeared in the cervical and in the inguinal lymph nodes, especially when using the LO28 strain. At this time, no production of IFN-b was detectable in the spleen any longer. Loss of the signal from the spleen 48 hours p.i. could be due to complete destruction of spleen together with the massive apoptosis of lymphocytes [32] . Quantitation of luciferase activity in the selected regions of interest (Fig. 1A , circles 1 and 2 for spleen and cervical lymph nodes, respectively) showed that LO28, induced a stronger signal compared to EGDe (Fig. 1B) , although colonization by bacteria was comparable (Fig. 1C) . This confirmed the findings by Reutterer et al. that LO28 is the most potent type I IFN stimulator amongst the commonly used Listeria strains [31] . Of note, there was no significant signal from the liver at any time point, although this organ is highly colonized by Listeria.