CEACAM1 induces B-cell survival and is essential for protective antiviral antibody production.
CEACAM1 induces B-cell survival and is essential for protective antiviral antibody production.
Nature communications (2015-02-19)
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 Marquardsen, Katja Merches, Elisabeth Lang, Carsten Kirschning, Astrid M Westendorf, Dieter Häussinger, Florian Lang, Ulf Dittmer, Ralf Küppers, Mike Recher, Cornelia Hardt, Inka Scheffrahn, Nicole Beauchemin, Joachim R Göthert, Bernhard B Singer, Philipp A Lang, Karl S Lang
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.
