Dickkopf-3 Acts as a Modulator of B Cell Fate and Function
Ludwig J, Federico G, Prokosch S, Kueblbeck G, Schmitt S, Klevenz A, Groene HJ, Nitschke L, Arnold B (2015)
Publication Status: Published
Publication Type: Journal article
Publication year: 2015
Journal
Publisher: AMER ASSOC IMMUNOLOGISTS
Book Volume: 194
Pages Range: 2624-2634
Journal Issue: 6
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 Ca2+ 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.
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Germany (DE)How to cite
APA:
Ludwig, J., Federico, G., Prokosch, S., Kueblbeck, G., Schmitt, S., Klevenz, A.,... Arnold, B. (2015). Dickkopf-3 Acts as a Modulator of B Cell Fate and Function. Journal of Immunology, 194(6), 2624-2634. https://dx.doi.org/10.4049/jimmunol.1402160
MLA:
Ludwig, Julia, et al. "Dickkopf-3 Acts as a Modulator of B Cell Fate and Function." Journal of Immunology 194.6 (2015): 2624-2634.
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