Aminobisphosphonates inhibit dendritic cell-mediated antigen-specific activation of CD1d-restricted iNKT cells

Aminobisphosphonates inhibit dendritic cell-mediated antigen-specific activation of CD1d-restricted iNKT cells

Copyright © 2015 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 158(2015), 1 vom: 28. Mai, Seite 92-9
1. Verfasser: Schneiders, Famke L (VerfasserIn)
Weitere Verfasser: Huijts, Charlotte M, Mantici, Aslihan, Menks, Mica A C, Scotet, Emmanuel, Veerhuis, Rob, Verheul, Henk M W, de Gruijl, Tanja D, van der Vliet, Hans J
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2015
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Aminobisphosphonates Apolipoprotein E (apoE) dendritic cell (DC) iNKT α-GalCer Amines Antigens, CD1d Bone Density Conservation Agents mehr... Diphosphonates Galactosylceramides alpha-galactosylceramide
Beschreibung
Zusammenfassung:Copyright © 2015 Elsevier Inc. All rights reserved.
CD1d-restricted invariant natural killer T (iNKT) cells constitute an important immunoregulatory T cell subset that can be activated by the synthetic glycolipid α-galactosylceramide (α-GalCer) and initiate antitumor immune responses. As cancer patients are frequently treated with aminobisphosphonates (NBP), it is relevant to determine possible effects of NBP on CD1d-restricted glycolipid Ag-presentation to iNKT cells. We report a striking reduction of α-GalCer-induced iNKT cell activation by monocyte derived dendritic cells (moDC) upon their exposure to NBP during maturation. We found that production of apolipoprotein E (apoE), which is a known facilitator of trans-membrane transport of exogenously derived glycolipids, was significantly diminished in moDC exposed to NBP. As the inhibitory effect of NBP on iNKT cell activation was alleviated by exogenous apoE, our data indicate that reduced apoE production by antigen presenting cells (APC) through NBP limits glycolipid-induced iNKT cell activation. This should be taken into account in the design of iNKT cell-based anti-cancer therapies
Beschreibung:Date Completed 07.07.2015
Date Revised 04.05.2015
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2015.03.007