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Salivary gland resident APCs are Flt3L- and CCR2-independent macrophage-like cells incapable of cross-presentation.

Authors
  • Thom, Jenny T
  • Walton, Senta M
  • Torti, Nicole
  • Oxenius, Annette
Type
Published Article
Journal
European Journal of Immunology
Publisher
Wiley
Publication Date
Mar 01, 2014
Volume
44
Issue
3
Pages
706–714
Identifiers
DOI: 10.1002/eji.201343992
PMID: 24271944
Source
Medline
Keywords
License
Unknown

Abstract

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-γ 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.

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