(TIF) Production of IFN-β during Listeria monocytogenes Infection Is Restricted to Monocyte/Macrophage Lineage The family of type I interferons (IFN), which consists of several IFN-α and one IFN-β, are produced not only after stimulation by viruses, but also after infection with non-viral pathogens. In the course of bacterial infections, these cytokines could be beneficial or detrimental. IFN-β is the primary member of type I IFN that initiates a cascade of IFN-α production. Here we addressed the question which cells are responsible for IFN-β expression after infection with the intracellular pathogen Listeria monocytogenes by using a genetic approach. By means of newly established reporter mice, maximum of IFN-β expression was observed at 24 hours post infection in spleen and, surprisingly, 48 hours post infection in colonized cervical and inguinal lymph nodes. Colonization of lymph nodes was independent of the type I IFN signaling, as well as bacterial dose and strain. Using cell specific reporter function and conditional deletions we could define cells expressing LysM as the major IFN-β producers, with cells formerly defined as Tip-DCs being the highest. Neutrophilic granulocytes, dendritic cells and plasmacytoid dendritic cells did not significantly contribute to type I IFN production. Interferons (IFN) were first discovered over 50 years ago by Isaacs and Lindenmann [1] . Due to its complexity, the IFN system is still little understood and remains a subject of intensive research. Currently, three types of IFNs are distinguished -type I, type II consisting of only IFN-c, and the recently discovered type III also called IFN-l. Here, we will focus on type I IFN. This family of cytokines comprises a single IFN-b, more than 13 IFN-a, and several other less well characterized members [2, 3] . All these subtypes signal through a common cell surface receptor (IFNAR) to activate IFN-inducible genes that exert a wide range of effects central to innate and adaptive immunity [2] . As a rule, IFN-b is produced as the earliest of type I IFN initiating a cascade of IFN-a via autocrine and paracrine loops [4, 5] . In addition, during viral infections type I IFN may be induced in plasmacytoid dendritic cells (pDCs) also named ''natural interferon producing cells''. Due to constitutive expression of the transcription factor IRF-7, pDCs are able to immediately produce large amounts of IFN-a [6] . Nonviral pathogens (i.e., bacteria, protozoa, fungi and helminthes) may also induce type I IFN. Interestingly, in contrast to viral infections where IFNs are normally protective, in non-viral infections IFN production might be defensive or deleterious [7, 8] .