Defective TLR9-driven STAT3 activation in B cells of patients with CVID

Bibliographische Detailangaben
Veröffentlicht in:	Clinical immunology (Orlando, Fla.). - 1999. - 197(2018) vom: 01. Dez., Seite 40-44
1. Verfasser:	Borzutzky, Arturo (VerfasserIn)
Weitere Verfasser:	Rauter, Ingrid, Fried, Ari, Rachid, Rima, McDonald, Douglas R, Hammarstrom, Lennart, Grimbacher, Bodo, Abraham, Roshini S, Geha, Raif S
Format:	Online-Aufsatz
Sprache:	English
Veröffentlicht:	2018
Zugriff auf das übergeordnete Werk:	Clinical immunology (Orlando, Fla.)
Schlagworte:	Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't B cells Common variable immunodeficiency STAT3 Transcription factor Toll-like Receptor 9 DNA, Bacterial Immunoglobulin G NF-kappa B mehr... Oligodeoxyribonucleotides STAT3 Transcription Factor STAT3 protein, human TLR9 protein, human Toll-Like Receptor 9

Beschreibung
Zusammenfassung:	Copyright © 2018 Elsevier Inc. All rights reserved. B cell activation by Toll-like receptor 9 (TLR9) ligands is dependent on STAT3 and is important for optimal antibody responses to microbial antigens. B cells from patients with common variable immune deficiency (CVID) have impaired proliferation and differentiation in response to the TLR9 ligand CpG, despite normal levels of TLR9 expression. We demonstrate that CpG-driven STAT3 phosphorylation, but not activation of NFκB and p38, is selectively impaired in B cells from CVID patients. These results suggest that defective STAT3 activation contributes to the defective TLR9 and antibody response of B cells in CVID
Beschreibung:	Date Completed 07.10.2019 Date Revised 07.10.2019 published: Print-Electronic Citation Status MEDLINE
ISSN:	1521-7035
DOI:	10.1016/j.clim.2018.08.008