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Event Abstract Back to Event Mzb1 protein regulates antibody secretion and integrin activation in innate-like B cells Virginia Andreani1*, Marc Rosenbaum1, Tanya Kapoor1 and Rudolf Grosschedl1 1 Max Planck Institute of Immunobiology and Epigenetics, Department of Cellular and Molecular Immunology, Germany Marginal zone (MZ) B cells of the spleen and B1 cells, termed innate-like B cells, differ from Follicular B cells by their attenuated Ca2+ mobilization, fast antibody secretion, and increased cell adhesion. We identified and characterized Mzb1 as an endoplasmic reticulum (ER)-localized and B cell-specific protein that is most abundantly expressed in innate-like B cells. Knockdown of Mzb1 in MZ B cells increased Ca2+ mobilization and reduced integrin-mediated cell adhesion. To gain further insight into the function of Mzb1 in vivo and to study its role in the humoral immune response, we have generated and analyzed Mzb1 knock out mice. To assess the function of Mzb1 in the initiation of an early response to blood-borne T-cell-independent type 2 (TI-2) antigens, we intravenously challenged Mzb1+/+ and Mzb1-/- mice with the TI-2 antigen TNP-Ficoll or Streptococcus pneumonia type 3 polysaccharide (S.p. PS). The immune response of Mzb1-/- mice was significantly reduced compared with Mzb1+/+ mice. We also detected in Mzb1-/- mice, reduced amounts of anti-TNP-specific antibodies of the IgG3 isotype, consistent with the role of MZ B cell in the generation of IgG3 in a TI-2 response. We could also demonstrate a reduced integrin activation and reduced adhesion capacity to the molecules ICAM1 and VCAM1, in Mzb1-/- MZ B cells compared to Mzb1 expressing wild type MZ B Cells. Together, these results suggest that the ER protein Mzb1, is important for immunoglobulin secretion and integrin-mediated adhesion. Keywords: Marginal zone B cells, Immunoglobulins, Integrins, Adhesion, Endoplasmic Reticulum Conference: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología, Medellin, Colombia, 13 Oct - 16 Oct, 2015. Presentation Type: Poster Presentation Topic: Innate Immunity Citation: Andreani V, Rosenbaum M, Kapoor T and Grosschedl R (2015). Mzb1 protein regulates antibody secretion and integrin activation in innate-like B cells. Front. Immunol. Conference Abstract: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología. doi: 10.3389/conf.fimmu.2015.05.00035 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 14 Apr 2015; Published Online: 14 Sep 2015. * Correspondence: Dr. Virginia Andreani, Max Planck Institute of Immunobiology and Epigenetics, Department of Cellular and Molecular Immunology, Freiburg, Freiburg, D-79108, Germany, virandreani@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Virginia Andreani Marc Rosenbaum Tanya Kapoor Rudolf Grosschedl Google Virginia Andreani Marc Rosenbaum Tanya Kapoor Rudolf Grosschedl Google Scholar Virginia Andreani Marc Rosenbaum Tanya Kapoor Rudolf Grosschedl PubMed Virginia Andreani Marc Rosenbaum Tanya Kapoor Rudolf Grosschedl Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

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