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

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Khairnar Vishal, Duhan Vikas, Maney Sathish Kumar, Honke Nadine, Shaabani Namir, Pandyra Aleksandra A, Seifert Marc, Pozdeev Vitaly, Xu Haifeng C, Sharma Piyush, Baldin Fabian, Marquardsen Florian, Merches Katja, Lang Elisabeth, Kirschning Carsten, Westendorf Astrid M, Häussinger Dieter, Lang Florian, Dittmer Ulf, Küppers Ralf, Recher Mike, Hardt Cornelia, Scheffrahn Inka, Beauchemin Nicole, Göthert Joachim R,
Project Analysis of RAG-dependent immunodeficiency and autoimmunity
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Original article (peer-reviewed)

Journal Nature communications
Volume (Issue) 6
Page(s) 6217 - 6217
Title of proceedings Nature communications
DOI 10.1038/ncomms7217

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.
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