| First Author | Thom JT | Year | 2014 |
| Journal | Eur J Immunol | Volume | 44 |
| Issue | 3 | Pages | 706-14 |
| PubMed ID | 24271944 | Mgi Jnum | J:209082 |
| Mgi Id | MGI:5565644 | Doi | 10.1002/eji.201343992 |
| Citation | Thom JT, et al. (2014) Salivary gland resident APCs are Flt3L- and CCR2-independent macrophage-like cells incapable of cross-presentation. Eur J Immunol 44(3):706-14 |
| abstractText | Cytomegaloviruses (CMVs) disseminate within the human population via mucosal excretions, for example, from the salivary glands (SGs), which represent a privileged site of viral immune evasion and persistence. The murine CMV (MCMV) model has served to identify factors that maintain a unique virus-host relationship in this organ. In contrast to all other organs, the SG is resistant to CD8(+) T-cell mediated control of MCMV replication due to virally induced MHC class I downregulation, which is exceptionally efficient in acinar glandular epithelial cells. Uniquely to the SG, IFN-gamma producing CD4(+) T cells are required for virus control. While T-cell responses have been extensively characterized in the SG, the ontogeny and function of APCs in this organ remain to be assessed. Here, we show that macrophage-like cells constitute the population of SG-resident APCs in steady state and during MCMV-induced inflammation in mice. Inflammatory monocytes, monocyte-derived DCs as well as conventional, Flt3L-dependent DCs do not contribute to this population. Despite supporting contact formation to CD4(+) and CD8(+) T cells in principle, SG-resident APCs fail to activate the latter due to their inability to cross-present MCMV-derived antigen. |
