NDLI: Dickkopf-3 acts as a modulator of B cell fate and function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gröne, Hermann-Josef Federico, Giuseppina Arnold, Bernd Klevenz, Alexandra Prokosch, Sandra Ludwig, Julia Küblbeck, Günter Schmitt, Sabine Nitschke, Lars
Description	Author Affiliation: Ludwig J ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany); Federico G ( Division of Cellular and Molecular Pathology, German Cancer Research Center, 69120 Heidelberg, Germany); Prokosch S ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany); Küblbeck G ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany); Schmitt S ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany); Klevenz A ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany); Gröne HJ ( Division of Cellular and Molecular Pathology, German Cancer Research Center, 69120 Heidelberg, Germany); Nitschke L ( Division of Genetics, Department of Biology, University of Erlangen, 91058 Erlangen, Germany.); Arnold B ( Division of Molecular Immunology, German Cancer Research Center, 69120 Heidelberg, Germany)
Abstract	The mechanisms responsible for the generation of a mature B1 and B2 cell compartment are still poorly understood. In this study, we demonstrated that absence of Dickkopf-3 (DKK3) led to changes in the composition of the B cell compartment, which were due to an altered development and maintenance program of B cells. Development of B2 cells was impaired at the pre- and immature B cell stage, resulting in decreased numbers of follicular B cells in adult DKK3-deficient mice. Furthermore, DKK3 limited B1 cell self-maintenance in the periphery, by decreasing the survival and proliferation behavior of B1 cells. DKK3 may act via the BCR signaling pathway, as Ca(2+) influx upon BCR stimulation was increased and SiglecG, a molecule shown to inhibit Calcium signaling, was downregulated in the absence of DKK3. DKK3-deficient mice exhibited altered Ab responses and an increased secretion of the cytokine IL-10. Additionally, DKK3 limited autoimmunity in a model of systemic lupus erythematosus. In summary, we identified DKK3 as a novel modulator interfering with B cell fate as well as the maintenance program of B cells, leading to changes in B cell immune responses.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	6
Volume Number	194
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-03-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	B-lymphocytes Immunology Cell Proliferation Intercellular Signaling Peptides And Proteins Signal Transduction Animals Apoptosis Genetics Autoantibodies Metabolism Calcium Cell Survival Cells, Cultured Cytokines Flow Cytometry Gene Expression Deficiency Lectins Lupus Erythematosus, Systemic Lymphocyte Count Mice, Inbred C57bl Mice, Inbred Mrl Lpr Mice, Knockout Receptors, Antigen, B-cell Reverse Transcriptase Polymerase Chain Reaction Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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