|  Help  |  About  |  Contact Us

Publication : Functional evaluation of activation-dependent alterations in the sialoglycan composition of T cells.

First Author  Naito-Matsui Y Year  2014
Journal  J Biol Chem Volume  289
Issue  3 Pages  1564-79
PubMed ID  24297165 Mgi Jnum  J:207174
Mgi Id  MGI:5554627 Doi  10.1074/jbc.M113.523753
Citation  Naito-Matsui Y, et al. (2014) Functional evaluation of activation-dependent alterations in the sialoglycan composition of T cells. J Biol Chem 289(3):1564-79
abstractText  Sialic acids (Sias) are often conjugated to the termini of cellular glycans and are key mediators of cellular recognition. Sias are nine-carbon acidic sugars, and, in vertebrates, the major species are N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc), differing in structure at the C5 position. Previously, we described a positive feedback loop involving regulation of Neu5Gc expression in mouse B cells. In this context, Neu5Gc negatively regulated B-cell proliferation, and Neu5Gc expression was suppressed upon activation. Similarly, resting mouse T cells expressed principally Neu5Gc, and Neu5Ac was induced upon activation. In the present work, we used various probes to examine sialoglycan expression by activated T cells in terms of the Sia species expressed and the linkages of Sias to glycans. Upon T-cell activation, sialoglycan expression shifted from Neu5Gc to Neu5Ac, and the linkage shifted from alpha2,6 to alpha2,3. These changes altered the expression levels of sialic acid-binding immunoglobulin-like lectin (siglec) ligands. Expression of sialoadhesin and Siglec-F ligands increased, and that of CD22 ligands decreased. Neu5Gc exerted a negative effect on T-cell activation, both in terms of the proliferative response and in the context of activation marker expression. Suppression of Neu5Gc expression in mouse T and B cells prevented the development of nonspecific CD22-mediated T cell-B cell interactions. Our results suggest that an activation-dependent shift from Neu5Gc to Neu5Ac and replacement of alpha2,6 by alpha2,3 linkages may regulate immune cell interactions at several levels.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression