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Rockefeller University Press, Journal of Experimental Medicine, 1(212), p. 53-72, 2014

DOI: 10.1084/jem.20141143

Rockefeller University Press, Journal of Cell Biology, 1(208), p. 2081OIA235

DOI: 10.1083/jcb.2081oia235

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Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity

Journal article published in 2014 by Marianne Burbage, Selina J. Keppler, Francesca Gasparrini, Nuria Martínez-Martín, Mauro Gaya, Christoph Feest, Marie-Charlotte Domart, Cord Brakebusch, Lucy Collinson ORCID, Andreas Bruckbauer, Facundo D. Batista
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The small Rho GTPase Cdc42, known to interact with Wiskott–Aldrich syndrome (WAS) protein, is an important regulator of actin remodeling. Here, we show that genetic ablation of Cdc42 exclusively in the B cell lineage is sufficient to render mice unable to mount antibody responses. Indeed Cdc42-deficient mice are incapable of forming germinal centers or generating plasma B cells upon either viral infection or immunization. Such severe immune deficiency is caused by multiple and profound B cell abnormalities, including early blocks during B cell development; impaired antigen-driven BCR signaling and actin remodeling; defective antigen presentation and in vivo interaction with T cells; and a severe B cell–intrinsic block in plasma cell differentiation. Thus, our study presents a new perspective on Cdc42 as key regulator of B cell physiology.