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    Immunoglobulin expression in the endoplasmic reticulum shapes the metabolic fitness of B lymphocytes (2020)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Jumaa, Huda
    Caganova, Marieta
    McAllister, Ellen J.
    Hoenig, Laura
    He, Xiaocui
    Saltukoglu, Deniz
    Brenker, Kathrin
    Köhler, Markus
    Leben, Ruth
    Hauser, Anja E.
    Niesner, Raluca (WE 2)
    Rajewsky, Klaus
    Reth, Michael
    Jellusova, Julia
    Quelle
    Life science alliance
    Bandzählung: 3
    Heftzählung: 6
    Seiten: Artikel e202000700
    ISSN: 2575-1077
    Sprache
    Englisch
    Verweise
    URL (Volltext): https://www.life-science-alliance.org/lookup/doi/10.26508/lsa.202000700
    DOI: 10.26508/lsa.202000700
    Pubmed: 32341085
    Kontakt
    Institut für Veterinär-Physiologie

    Oertzenweg 19 b
    14163 Berlin
    +49 30 838 62600
    physiologie@vetmed.fu-berlin.de

    Abstract / Zusammenfassung

    The major function of B lymphocytes is to sense antigens and to produce protective antibodies after activation. This function requires the expression of a B-cell antigen receptor (BCR), and evolutionary conserved mechanisms seem to exist that ensure that B cells without a BCR do not develop nor survive in the periphery. Here, we show that the loss of BCR expression on Burkitt lymphoma cells leads to decreased mitochondrial function and impaired metabolic flexibility. Strikingly, this phenotype does not result from the absence of a classical Syk-dependent BCR signal but rather from compromised ER expansion. We show that the reexpression of immunoglobulins (Ig) in the absence of the BCR signaling subunits Igα and Igβ rescues the observed metabolic defects. We demonstrate that immunoglobulin expression is needed to maintain ER homeostasis not only in lymphoma cells but also in resting B cells. Our study provides evidence that the expression of BCR components, which is sensed in the ER and shapes mitochondrial function, represents a novel mechanism of metabolic control in B cells.