| Legionella pneumophila remains an important opportunistic pathogen of human macrophages. Its limited ability to replicate in murine macrophages has been attributed to redundant innate sensor systems that detect and effectively respond to this infection. The current studies evaluate the role of one of these innate response systems, the type I Interferon (IFN-I) autocrine loop. The ability of L. pneumophila to induce IFN-I expression was found to be dependent on IRF-3. Secreted IFN-Is then in turn suppress the intracellular replication of L. pneumophila . Surprisingly, this suppression is mediated by a pathway that is independent of Stat1, Stat2, and Stat3, but correlates with polarization of macrophages towards the M1 or classically activated phenotype. Investigation of this unique STAT independent pathway has revealed a new Stat1 independent activation pathway of Interferon Stimulated Genes (ISGs). |
