Journal Article DKFZ-2017-03066
Dickkopf-3 acts as a modulator of B cell fate and function.

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Soc. Bethesda, Md.

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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.

Keyword(s): Autoantibodies ; Cytokines ; Dkk3 protein, mouse ; Intercellular Signaling Peptides and Proteins ; Lectins ; Receptors, Antigen, B-Cell ; Siglecg protein, mouse ; Calcium


Contributing Institute(s):
  1. Zelluläre und Molekulare Pathologie (G130)
  2. B-Zell-Immunologie (D130)
Research Program(s):
  1. 314 - Tumor immunology (POF3-314) (POF3-314)

Appears in the scientific report 2015
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Medline ; BIOSIS Previews ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection
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 Record created 2017-09-21, last modified 2022-03-13

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