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

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Standard

Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity. / Burbage, Marianne; Keppler, Selina J; Gasparrini, Francesca; Martínez-Martín, Nuria; Gaya, Mauro; Feest, Christoph; Domart, Marie-Charlotte; Brakebusch, Cord Herbert; Collinson, Lucy; Bruckbauer, Andreas; Batista, Facundo D.

In: The Journal of Experimental Medicine, Vol. 212, No. 1, 2015, p. 53-72.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Burbage, M, Keppler, SJ, Gasparrini, F, Martínez-Martín, N, Gaya, M, Feest, C, Domart, M-C, Brakebusch, CH, Collinson, L, Bruckbauer, A & Batista, FD 2015, 'Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity', The Journal of Experimental Medicine, vol. 212, no. 1, pp. 53-72. https://doi.org/10.1084/jem.20141143

APA

Burbage, M., Keppler, S. J., Gasparrini, F., Martínez-Martín, N., Gaya, M., Feest, C., Domart, M-C., Brakebusch, C. H., Collinson, L., Bruckbauer, A., & Batista, F. D. (2015). Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity. The Journal of Experimental Medicine, 212(1), 53-72. https://doi.org/10.1084/jem.20141143

Vancouver

Burbage M, Keppler SJ, Gasparrini F, Martínez-Martín N, Gaya M, Feest C et al. Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity. The Journal of Experimental Medicine. 2015;212(1):53-72. https://doi.org/10.1084/jem.20141143

Author

Burbage, Marianne ; Keppler, Selina J ; Gasparrini, Francesca ; Martínez-Martín, Nuria ; Gaya, Mauro ; Feest, Christoph ; Domart, Marie-Charlotte ; Brakebusch, Cord Herbert ; Collinson, Lucy ; Bruckbauer, Andreas ; Batista, Facundo D. / Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity. In: The Journal of Experimental Medicine. 2015 ; Vol. 212, No. 1. pp. 53-72.

Bibtex

@article{c0b28b4b817b4aeeb4adbe6d24ffc747,
title = "Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity",
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.",
author = "Marianne Burbage and Keppler, {Selina J} and Francesca Gasparrini and Nuria Mart{\'i}nez-Mart{\'i}n and Mauro Gaya and Christoph Feest and Marie-Charlotte Domart and Brakebusch, {Cord Herbert} and Lucy Collinson and Andreas Bruckbauer and Batista, {Facundo D}",
note = "{\textcopyright} 2015 Burbage et al.",
year = "2015",
doi = "10.1084/jem.20141143",
language = "English",
volume = "212",
pages = "53--72",
journal = "The Journal of Experimental Medicine",
issn = "0022-1007",
publisher = "Rockefeller University Press",
number = "1",

}

RIS

TY - JOUR

T1 - Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity

AU - Burbage, Marianne

AU - Keppler, Selina J

AU - Gasparrini, Francesca

AU - Martínez-Martín, Nuria

AU - Gaya, Mauro

AU - Feest, Christoph

AU - Domart, Marie-Charlotte

AU - Brakebusch, Cord Herbert

AU - Collinson, Lucy

AU - Bruckbauer, Andreas

AU - Batista, Facundo D

N1 - © 2015 Burbage et al.

PY - 2015

Y1 - 2015

N2 - 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.

AB - 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.

U2 - 10.1084/jem.20141143

DO - 10.1084/jem.20141143

M3 - Journal article

C2 - 25547673

VL - 212

SP - 53

EP - 72

JO - The Journal of Experimental Medicine

JF - The Journal of Experimental Medicine

SN - 0022-1007

IS - 1

ER -

ID: 129627425