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Absence of Siglec-H in MCMV infection elevates interferon alpha production but does not enhance viral clearance.
Puttur, Franz Arnold-Schrauf, Catharina Lahl, Katharina Solmaz, Gulhas Lindenberg, Marc Mayer, Christian Thomas Gohmert, Melanie Swallow, Maxine van Helt, Christopher Schmitt, Heike
Puttur, Franz
Arnold-Schrauf, Catharina
Lahl, Katharina
Solmaz, Gulhas
Lindenberg, Marc
Mayer, Christian Thomas
Gohmert, Melanie
Swallow, Maxine
van Helt, Christopher
Schmitt, Heike
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2013-09
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Plasmacytoid dendritic cells (pDCs) express the I-type lectin receptor Siglec-H and produce interferon α (IFNα), 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 IFNα levels following systemic MCMV infection. Although Siglec-H modulates anti-viral IFNα 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.
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Absence of Siglec-H in MCMV infection elevates interferon alpha production but does not enhance viral clearance. 2013, 9 (9):e1003648 PLoS Pathog.
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en
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1553-7374
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