Genetic loss of NFAT2 (NFATc1) impairs B cell development of B1 and B2 B cells.

Cell Immunol

Dept. of Hematology, Oncology and Immunology, University Hospital Tübingen, Tübingen, Germany; Dept. of Hematology, Oncology and Immunology, Klinikum Region Hannover, KRH Klinikum Siloah, Hannover, Germany. Electronic address:

Published: March 2020

AI Article Synopsis

  • * Deleting NFAT2 impairs the development of B1 B cells, resulting in fewer B1 progenitors in the bone marrow and spleen, while leading to an increase in immature B cells and a decrease in marginal zone B cells.
  • * The study shows that NFAT2 regulates key markers and genes in B cells, impacting their proliferation and survival, thus providing significant insights into its role in B lymphocyte development in the periphery.

Article Abstract

NFAT2 activity was shown to be of critical importance in B cell receptor signaling, development and proliferation; however its role in B cell development in the periphery is still not completely understood. We confirmed that NFAT2 deletion leads to impaired B1 B cell development, supported by our finding of limited B1 progenitors in the bone marrow and spleen of NFAT2 deficient mice. Moreover, we show for the first time that loss of NFAT2 increases immature B cells in particular transitional T2 and T3 as well as mature follicular B cells while marginal zone B cells are decreased. We further demonstrate that NFAT2 regulates the expression of B220, CD23, CD38, IgM/IgD and ZAP70 in murine B cells. In vivo analyses revealed decreased proliferation and increased apoptosis of NFAT2 deficient B cells. In summary, this study provides an extensive analysis of the role of NFAT2 in peripheral B lymphocyte development.

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Source
http://dx.doi.org/10.1016/j.cellimm.2020.104048DOI Listing

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