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CEACAM1 induces B-cell survival and is essential for protective antiviral antibody production

Author

Listed:
  • Vishal Khairnar

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen)

  • Vikas Duhan

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen)

  • Sathish Kumar Maney

    (Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Nadine Honke

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen
    Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Namir Shaabani

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen
    Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Aleksandra A. Pandyra

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen)

  • Marc Seifert

    (Institute of Cell Biology (Cancer Research), University of Duisburg-Essen)

  • Vitaly Pozdeev

    (Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Haifeng C. Xu

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen
    Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Piyush Sharma

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen)

  • Fabian Baldin

    (Clinic for Primary Immunodeficiency, Medical Outpatient Unit and Immunodeficiency Laboratory, University Hospital)

  • Florian Marquardsen

    (Clinic for Primary Immunodeficiency, Medical Outpatient Unit and Immunodeficiency Laboratory, University Hospital)

  • Katja Merches

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen
    University of Tuebingen)

  • Elisabeth Lang

    (Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Carsten Kirschning

    (Institute of Medical Microbiology, Faculty of Medicine, University Hospital Essen)

  • Astrid M. Westendorf

    (Institute of Medical Microbiology, Faculty of Medicine, University Hospital Essen)

  • Dieter Häussinger

    (Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

  • Florian Lang

    (University of Tuebingen)

  • Ulf Dittmer

    (Institute of Virology, University of Duisburg-Essen)

  • Ralf Küppers

    (Institute of Cell Biology (Cancer Research), University of Duisburg-Essen)

  • Mike Recher

    (Clinic for Primary Immunodeficiency, Medical Outpatient Unit and Immunodeficiency Laboratory, University Hospital)

  • Cornelia Hardt

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen)

  • Inka Scheffrahn

    (Clinic of Gastroenterology and Hepatology, University of Duisburg-Essen)

  • Nicole Beauchemin

    (Rosalind and Morris Goodman Cancer Centre, Medicine and Oncology, McIntyre Medical Science Building)

  • Joachim R. Göthert

    (West German Cancer Center (WTZ), University Hospital Essen)

  • Bernhard B. Singer

    (Institute of Anatomy, Medical Faculty, University of Duisburg-Essen)

  • Philipp A. Lang

    (Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University
    Heinrich Heine University Düsseldorf)

  • Karl S. Lang

    (Institute of Immunology, Medical Faculty, University of Duisburg-Essen
    Clinic of Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University)

Abstract

B cells are essential for antiviral immune defence because they produce neutralizing antibodies, present antigen and maintain the lymphoid architecture. Here we show that intrinsic signalling of CEACAM1 is essential for generating efficient B-cell responses. Although CEACAM1 exerts limited influence on the proliferation of B cells, expression of CEACAM1 induces survival of proliferating B cells via the BTK/Syk/NF-κB-axis. The absence of this signalling cascade in naive Ceacam1−/− mice limits the survival of B cells. During systemic infection with cytopathic vesicular stomatitis virus, Ceacam1−/− mice can barely induce neutralizing antibody responses and die early after infection. We find, therefore, that CEACAM1 is a crucial regulator of B-cell survival, influencing B-cell numbers and protective antiviral antibody responses.

Suggested Citation

  • Vishal Khairnar & Vikas Duhan & Sathish Kumar Maney & Nadine Honke & Namir Shaabani & Aleksandra A. Pandyra & Marc Seifert & Vitaly Pozdeev & Haifeng C. Xu & Piyush Sharma & Fabian Baldin & Florian Ma, 2015. "CEACAM1 induces B-cell survival and is essential for protective antiviral antibody production," Nature Communications, Nature, vol. 6(1), pages 1-13, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7217
    DOI: 10.1038/ncomms7217
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