| First Author | Solodova E | Year | 2011 |
| Journal | PLoS One | Volume | 6 |
| Issue | 4 | Pages | e18543 |
| PubMed ID | 21494554 | Mgi Jnum | J:172226 |
| Mgi Id | MGI:5005017 | Doi | 10.1371/journal.pone.0018543 |
| Citation | Solodova E, et al. (2011) Production of IFN-beta during Listeria monocytogenes infection is restricted to monocyte/macrophage lineage. PLoS One 6(4):e18543 |
| abstractText | The family of type I interferons (IFN), which consists of several IFN-alpha and one IFN-beta, 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-beta is the primary member of type I IFN that initiates a cascade of IFN-alpha production. Here we addressed the question which cells are responsible for IFN-beta expression after infection with the intracellular pathogen Listeria monocytogenes by using a genetic approach. By means of newly established reporter mice, maximum of IFN-beta 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-beta 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. |
