Glutamate signaling through the kainate receptor enhances human immunoglobulin production

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

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

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.

Original languageEnglish
Pages (from-to)80-89
Number of pages10
JournalJournal of Neuroimmunology
Volume233
Issue number1-2
DOIs
StatePublished - Apr 2011

Bibliographical 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.

Keywords

  • ADAM10
  • B cell
  • CD23
  • Glutamate
  • Immunoglobulin
  • Kainate receptor

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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