| First Author | Puttur F | Year | 2013 |
| Journal | PLoS Pathog | Volume | 9 |
| Issue | 9 | Pages | e1003648 |
| PubMed ID | 24086137 | Mgi Jnum | J:214874 |
| Mgi Id | MGI:5604162 | Doi | 10.1371/journal.ppat.1003648 |
| Citation | Puttur F, et al. (2013) Absence of Siglec-H in MCMV infection elevates interferon alpha production but does not enhance viral clearance. PLoS Pathog 9(9):e1003648 |
| abstractText | Plasmacytoid dendritic cells (pDCs) express the I-type lectin receptor Siglec-H and produce interferon alpha (IFNalpha), a critical anti-viral cytokine during the acute phase of murine cytomegalovirus (MCMV) infection. The ligands and biological functions of Siglec-H still remain incompletely defined in vivo. Thus, we generated a novel bacterial artificial chromosome (BAC)-transgenic "pDCre" mouse which expresses Cre recombinase under the control of the Siglec-H promoter. By crossing these mice with a Rosa26 reporter strain, a representative fraction of Siglec-H(+) pDCs is terminally labeled with red fluorescent protein (RFP). Interestingly, systemic MCMV infection of these mice causes the downregulation of Siglec-H surface expression. This decline occurs in a TLR9- and MyD88-dependent manner. To elucidate the functional role of Siglec-H during MCMV infection, we utilized a novel Siglec-H deficient mouse strain. In the absence of Siglec-H, the low infection rate of pDCs with MCMV remained unchanged, and pDC activation was still intact. Strikingly, Siglec-H deficiency induced a significant increase in serum IFNalpha levels following systemic MCMV infection. Although Siglec-H modulates anti-viral IFNalpha production, the control of viral replication was unchanged in vivo. The novel mouse models will be valuable to shed further light on pDC biology in future studies. |
