| First Author | Piersma SJ | Year | 2020 |
| Journal | Elife | Volume | 9 |
| PubMed ID | 32723479 | Mgi Jnum | J:302391 |
| Mgi Id | MGI:6508240 | Doi | 10.7554/eLife.56882 |
| Citation | Piersma SJ, et al. (2020) Virus infection is controlled by hematopoietic and stromal cell sensing of murine cytomegalovirus through STING. Elife 9:e56882 |
| abstractText | Recognition of DNA viruses, such as cytomegaloviruses (CMVs), through pattern-recognition receptor (PRR) pathways involving MyD88 or STING constitute a first-line defense against infections mainly through production of type I interferon (IFN-I). However, the role of these pathways in different tissues is incompletely understood, an issue particularly relevant to the CMVs which have broad tissue tropisms. Herein, we contrasted anti-viral effects of MyD88 versus STING in distinct cell types that are infected with murine CMV (MCMV). Bone marrow chimeras revealed STING-mediated MCMV control in hematological cells, similar to MyD88. However, unlike MyD88, STING also contributed to viral control in non-hematological, stromal cells. Infected splenic stromal cells produced IFN-I in a cGAS-STING-dependent and MyD88-independent manner, while we confirmed plasmacytoid dendritic cell IFN-I had inverse requirements. MCMV-induced natural killer cytotoxicity was dependent on MyD88 and STING. Thus, MyD88 and STING contribute to MCMV control in distinct cell types that initiate downstream immune responses. |
