NDLI: Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.

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Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Riboldi, Elena Gilfillan, Susan Trinchieri, Giorgio Colonna, Marco Kim, Alfred H. J. Swiecki, Melissa Wang, Yaming Dzutsev, Amiran Vermi, William Ruedl, Christiane
Description	Author Affiliation: Swiecki M ( Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110)
Abstract	Plasmacytoid dendritic cells (pDC) produce IFN-I in response to viruses and are routinely identified in mice by SiglecH expression. SiglecH is a sialic acid-binding Ig-like lectin that has an immunomodulatory role during viral infections. In this study, we evaluated the impact of SiglecH deficiency on cytokine responses in the presence and absence of pDC. We found that lack of SiglecH enhanced IFN-I responses to viral infection, regardless of whether pDC were depleted. We also examined the expression pattern of SiglecH and observed that it was expressed by specialized macrophages and progenitors of classical dendritic cells and pDC. Accordingly, marginal zone macrophages and pDC precursors were eliminated in newly generated SiglecH-diphtheria toxin receptor (DTR)-transgenic (Tg) mice but not in CLEC4C-DTR-Tg mice after diphtheria toxin (DT) treatment. Using two bacterial models, we found that SiglecH-DTR-Tg mice injected with DT had altered bacterial uptake and were more susceptible to lethal Listeria monocytogenes infection than were DT-treated CLEC4C-DTR-Tg mice. Taken together, our findings suggest that lack of SiglecH may affect cytokine responses by cell types other than pDC during viral infections, perhaps by altering viral distribution or burden, and that cell depletion in SiglecH-DTR-Tg mice encompasses more than pDC.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1303135
Journal	The Journal of Immunology
Issue Number	9
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dendritic Cells Immunology Intercellular Signaling Peptides And Proteins Biosynthesis Lectins Genetics Receptors, Cell Surface Animals Cell Separation Cytokines Diphtheria Toxin Metabolism Enzyme-linked Immunosorbent Assay Flow Cytometry Fluorescent Antibody Technique Gene Knock-in Techniques Heparin-binding Egf-like Growth Factor Immunohistochemistry Infection Macrophages Mice Mice, Inbred C57bl Mice, Transgenic Reverse Transcriptase Polymerase Chain Reaction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells 1

This information is current as Plasmacytoid Dendritic Cells of SiglecH Encompasses More Than ControlDiphtheria Toxin Receptor under the Cell Depletion in Mice That Express

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Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.

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Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells 1

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Cell depletion in mice that express diphtheria toxin receptor under the control of SiglecH encompasses more than plasmacytoid dendritic cells.