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Title
Sialic Acid-Binding Immunoglobulin-like Lectin G Promotes Atherosclerosis and Liver Inflammation by Suppressing the Protective Functions of B-1 Cells
AuthorBinder, Christoph J. ; Nitschke, Lars ; Shiri-Sverdlov, Ronit ; Witztum, Joseph L. ; Mallat, Ziad ; Goederle, Laura ; Ozsvar-Kozma, Maria ; Tsiantoulas, Dimitrios ; Hendrikx, Tim ; Gruber, Sabrina
Published in
Cell Reports, Cambridge, 2016, Vol. 14, Issue 10, page 2348-2361
PublishedCambridge : Cell Press, 2016
LanguageEnglish
Document typeJournal Article
Keywords (EN)oxidation-specific epitopes / low-density-lipoprotein / g deficiency leads / siglec-g / apoptotic cells / b-lymphocytes / nonalcoholic steatohepatitis / natural antibodies / innate immunity / oxidized ldl
Project-/ReportnumberF 5402-B21
ISSN2211-1247
URNurn:nbn:at:at-ubmuw:3-1865 Persistent Identifier (URN)
DOI10.1016/j.celrep.2016.02.027 
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Sialic Acid-Binding Immunoglobulin-like Lectin G Promotes Atherosclerosis and Liver Inflammation by Suppressing the Protective Functions of B-1 Cells [2.96 mb]
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Abstract (English)

Atherosclerosis is initiated and sustained by hypercholesterolemia, which results in the generation of oxidized LDL (OxLDL) and other metabolic byproducts that trigger inflammation. Specific immune responses have been shown to modulate the inflammatory response during atherogenesis. The sialic acid-binding immunoglobulin-like lectin G (Siglec-G) is a negative regulator of the functions of several immune cells, including myeloid cells and B-1 cells. Here, we show that deficiency of Siglec-G in atherosclerosis-prone mice inhibits plaque formation and diet-induced hepatic inflammation. We further demonstrate that selective deficiency of Siglec-G in B cells alone is sufficient to mediate these effects. Levels of B-1 cell-derived natural IgM with specificity for OxLDL were significantly increased in the plasma and peritoneal cavity of Siglec-G-deficient mice. Consistent with the neutralizing functions of OxLDL-specific IgM, Siglec-G-deficient mice were protected from OxLDL-induced sterile inflammation. Thus, Siglec-G promotes atherosclerosis and hepatic inflammation by suppressing protective anti-inflammatory effector functions of B cells.

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CC-BY-License (4.0)Creative Commons Attribution 4.0 International License