A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

Elizabeth Clayton; Giuseppe Bardi; Sarah E. Bell; David Chantry; Charles Downes; Alexander Gray; Lisa A. Humphries; David Rawlings; Helen Reynolds; Elena Vigorito; Martin Turner

doi:10.1084/jem.20020805

A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

Elizabeth Clayton
, Giuseppe Bardi
, Sarah E. Bell
, David Chantry
, Charles Downes
, Alexander Gray
, Lisa A. Humphries
, David Rawlings
, Helen Reynolds
, Elena Vigorito
, Martin Turner

Research output: Contribution to journal › Article › peer-review

411 Citations (Scopus)

Abstract

Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ^-/- B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.

Original language	English
Pages (from-to)	753-763
Number of pages	11
Journal	Journal of Experimental Medicine
Volume	196
Issue number	6
DOIs	https://doi.org/10.1084/jem.20020805
Publication status	Published - 9 Sept 2002

Keywords

Akt
Btk
Calcium
Gene targeting
p110δ

ASJC Scopus subject areas

Immunology and Allergy
Immunology

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10.1084/jem.20020805

Cite this

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title = "A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation",

abstract = "Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ-/- B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.",

keywords = "Akt, Btk, Calcium, Gene targeting, p110δ",

author = "Elizabeth Clayton and Giuseppe Bardi and Bell, \{Sarah E.\} and David Chantry and Charles Downes and Alexander Gray and Humphries, \{Lisa A.\} and David Rawlings and Helen Reynolds and Elena Vigorito and Martin Turner",

year = "2002",

month = sep,

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doi = "10.1084/jem.20020805",

language = "English",

volume = "196",

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journal = "Journal of Experimental Medicine",

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TY - JOUR

T1 - A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

AU - Clayton, Elizabeth

AU - Bardi, Giuseppe

AU - Bell, Sarah E.

AU - Chantry, David

AU - Downes, Charles

AU - Gray, Alexander

AU - Humphries, Lisa A.

AU - Rawlings, David

AU - Reynolds, Helen

AU - Vigorito, Elena

AU - Turner, Martin

PY - 2002/9/9

Y1 - 2002/9/9

N2 - Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ-/- B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.

AB - Mice lacking the p110δ catalytic subunit of phosphatidylinositol 3-kinase have reduced numbers of B1 and marginal zone B cells, reduced levels of serum immunoglobulins, respond poorly to immunization with type II thymus-independent antigen, and are defective in their primary and secondary responses to thymus-dependent antigen. p110δ-/- B cells proliferate poorly in response to B cell receptor (BCR) or CD40 signals in vitro, fail to activate protein kinase B, and are prone to apoptosis. p110δ function is required for BCR-mediated calcium flux, activation of phosphlipaseCγ2, and Bruton's tyrosine kinase. Thus, p110δ plays a critical role in B cell homeostasis and function.

KW - Akt

KW - Btk

KW - Calcium

KW - Gene targeting

KW - p110δ

U2 - 10.1084/jem.20020805

DO - 10.1084/jem.20020805

M3 - Article

C2 - 12235209

AN - SCOPUS:0037119630

SN - 0022-1007

VL - 196

SP - 753

EP - 763

JO - Journal of Experimental Medicine

JF - Journal of Experimental Medicine

IS - 6

ER -

A crucial role for the p110δ subunit of phosphatidylinositol 3-kinase in B cell development and activation

Abstract

Keywords

ASJC Scopus subject areas

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