CD161 receptor participates in both impairing NK cell cytotoxicity and the response to glycans and vimentin in patients with rheumatoid arthritis

(c) 2010 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 136(2010), 1 vom: 03. Juli, Seite 139-47
1. Verfasser: Richter, J (VerfasserIn)
Weitere Verfasser: Benson, V, Grobarova, V, Svoboda, J, Vencovsky, J, Svobodova, R, Fiserova, A
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2010
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Autoantibodies Autoantigens Glucocorticoids Glycoconjugates Immunosuppressive Agents NK Cell Lectin-Like Receptor Subfamily B Polysaccharides Vimentin mehr... N-Acetylglucosaminyltransferases EC 2.4.1.- alpha-1,6-mannosylglycoprotein beta 1,6-N-acetylglucosaminyltransferase EC 2.4.1.155 Hydrolases EC 3.- PADI4 protein, human EC 3.5.3.15 Protein-Arginine Deiminase Type 4 Protein-Arginine Deiminases
Beschreibung
Zusammenfassung:(c) 2010 Elsevier Inc. All rights reserved.
We investigated the role of natural killer (NK) cells and CD161, their primary C-type-lectin-like receptor in rheumatoid arthritis (RA). Samples were compared with healthy donors (HD), dermatomyositic (DM), polymyositic (PM), and osteoarthritic (OA) patients. RA, PM, and DM NK cell cytotoxicities significantly decreased relative to the HD and OA NK cells (p<0.0001). These results correlated with an increased expression of NK cell inhibitory receptor CD161, in active disease RA patients. We demonstrated that NK cells are able to respond to mutated citrullinated vimentin (MCV), an RA-specific autoantigen, leading to increases in both PAD4 enzyme and CD161 mRNA expression. MGAT5 glycosidase involvement was detected in GlcNAc metabolism within the synoviocytes of RA patients. Our findings reveal a functional relationship between CD161 expression and NK cell cytotoxicity as well as reactivity to glycans and MCV, thus providing new insight into the pathogenesis of RA and confirming the involvement of surface glycosylation
Beschreibung:Date Completed 06.08.2010
Date Revised 10.12.2019
published: Print-Electronic
ErratumIn: Clin Immunol. 2015 Mar;157(1):102
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2010.03.005