Glutamate signaling through the kainate receptor enhances human immunoglobulin production

Jamie L. Sturgill; Joel Mathews; Peggy Scherle; Daniel H. Conrad

doi:10.1016/j.jneuroim.2010.11.014

Glutamate signaling through the kainate receptor enhances human immunoglobulin production

Jamie L. Sturgill
, Joel Mathews
, Peggy Scherle
, Daniel H. Conrad

Producción científica: Article › revisión exhaustiva

29 Citas (Scopus)

Resumen

CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation.

Idioma original	English
Páginas (desde-hasta)	80-89
Número de páginas	10
Publicación	Journal of Neuroimmunology
Volumen	233
N.º	1-2
DOI	https://doi.org/10.1016/j.jneuroim.2010.11.014
Estado	Published - abr 2011

Nota bibliográfica

Funding Information:
The authors would like to thank Rebecca Martin for excellent technical assistance and Drs. John Tew and Suzanne Barbour for critical review of the manuscript. Grants U19AI077435 and RO1AI18697 from NIH/NIAID provided support for these studies. Imaging cytometry supported in part by NIH Grant P30 CA16059.

Financiación

The authors would like to thank Rebecca Martin for excellent technical assistance and Drs. John Tew and Suzanne Barbour for critical review of the manuscript. Grants U19AI077435 and RO1AI18697 from NIH/NIAID provided support for these studies. Imaging cytometry supported in part by NIH Grant P30 CA16059.

Financiadores	Número del financiador
National Institutes of Health (NIH)	P30 CA16059
National Institute of Allergy and Infectious Diseases	R01AI018697

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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10.1016/j.jneuroim.2010.11.014

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title = "Glutamate signaling through the kainate receptor enhances human immunoglobulin production",

abstract = "CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation.",

keywords = "ADAM10, B cell, CD23, Glutamate, Immunoglobulin, Kainate receptor",

author = "Sturgill, \{Jamie L.\} and Joel Mathews and Peggy Scherle and Conrad, \{Daniel H.\}",

note = "Funding Information: The authors would like to thank Rebecca Martin for excellent technical assistance and Drs. John Tew and Suzanne Barbour for critical review of the manuscript. Grants U19AI077435 and RO1AI18697 from NIH/NIAID provided support for these studies. Imaging cytometry supported in part by NIH Grant P30 CA16059.",

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AU - Sturgill, Jamie L.

AU - Mathews, Joel

AU - Scherle, Peggy

AU - Conrad, Daniel H.

N1 - Funding Information: The authors would like to thank Rebecca Martin for excellent technical assistance and Drs. John Tew and Suzanne Barbour for critical review of the manuscript. Grants U19AI077435 and RO1AI18697 from NIH/NIAID provided support for these studies. Imaging cytometry supported in part by NIH Grant P30 CA16059.

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N2 - CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation.

AB - CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation.

KW - ADAM10

KW - B cell

KW - CD23

KW - Glutamate

KW - Immunoglobulin

KW - Kainate receptor

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U2 - 10.1016/j.jneuroim.2010.11.014

DO - 10.1016/j.jneuroim.2010.11.014

M3 - Article

C2 - 21215464

AN - SCOPUS:79953301329

SN - 0165-5728

VL - 233

SP - 80

EP - 89

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Glutamate signaling through the kainate receptor enhances human immunoglobulin production

Resumen

Nota bibliográfica

Financiación

ASJC Scopus subject areas

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