Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 212, Issue 1, Pages 53-72Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20141143
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Funding
- Cancer Research UK
- German Research Foundation [Ke1737/1-1]
- Institute Pasteur-Fondazione Cenci Bolognetti
- EMBO
- Royal Society Wolfson Research Merit Award
- Cancer Research UK [15691] Funding Source: researchfish
- The Francis Crick Institute [10004, 10035] Funding Source: researchfish
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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.
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