Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity
Research output: Contribution to journal › Journal article › Research › peer-review
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.
Original language | English |
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Journal | The Journal of Experimental Medicine |
Volume | 212 |
Issue number | 1 |
Pages (from-to) | 53-72 |
ISSN | 0022-1007 |
DOIs | |
Publication status | Published - 2015 |
ID: 129627425