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Cochaperone Mzb1 is a key effector of Blimp1 in plasma cell differentiation and β1-integrin function

MPG-Autoren

Andreani,  Virginia
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Ramamoorthy,  Senthilkumar
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Pandey,  Abhinav
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Lupar,  Ekaterina
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Lämmermann,  Tim
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Grosschedl,  Rudolf
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

Externe Ressourcen

https://www.pnas.org/content/115/41/E9630.long
(Verlagsversion)

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Zitation

Andreani, V., Ramamoorthy, S., Pandey, A., Lupar, E., Nutt, S. L., Lämmermann, T., et al. (2018). Cochaperone Mzb1 is a key effector of Blimp1 in plasma cell differentiation and β1-integrin function. Proceedings of the National Academy of Sciences of the United States of America, 115, E9630-E9639. doi:10.1073/pnas.1809739115.


Zitierlink: https://hdl.handle.net/21.11116/0000-0002-C2AE-F
Zusammenfassung
Plasma cell differentiation involves coordinated changes in gene expression and functional properties of B cells. Here, we study the role of Mzb1, a Grp94 cochaperone that is expressed in marginal zone (MZ) B cells and during the terminal differentiation of B cells to antibody-secreting cells. By analyzing Mzb1-/- Prdm1 +/gfp mice, we find that Mzb1 is specifically required for the differentiation and function of antibody-secreting cells in a T cell-independent immune response. We find that Mzb1-deficiency mimics, in part, the phenotype of Blimp1 deficiency, including the impaired secretion of IgM and the deregulation of Blimp1 target genes. In addition, we find that Mzb1-/-plasmablasts show a reduced activation of β1-integrin, which contributes to the impaired plasmablast differentiation and migration of antibody-secreting cells to the bone marrow. Thus, Mzb1 function is required for multiple aspects of plasma cell differentiation.