English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Many non-classical, or class Ib, MHC molecules, including those linked to the cell membrane via glycosylphosphatidylinositol (GPI) membrane anchors, are poor stimulators of primary cytotoxic T cell responses. Some studies have suggested that certain amino acid substitutions in the alpha 3 domains of class Ib molecules may adversely affect their ability to interact with CD8, thereby affecting their ability to stimulate CD8+ T cells. In this report we show that poor stimulation by GPI-linked class I MHC molecules is not simply due to a failure to interact with CD8, but to a fundamental difference in the way T cells respond to GPI-anchored class I molecules. We have demonstrated this in two ways. Firstly, we have shown that GPI-linked H-2Kb molecules in which the amino acid sequence of the alpha 3 domain is identical to that of transmembrane H-2Kb remain less effective stimulators of a primary T cell response than membrane-spanning H-2Kb molecules. Secondly, using CD8- responder T cell hybridomas and responder T cells from transgenic mice expressing a CD8-independent TCR, we can show that the poor stimulatory ability of GPI-linked H-2Kb molecules is unrelated to their ability to interact with either CD8 or the TCR. These results suggest that the transmembrane linkage of class I MHC molecules plays an important role in the initial priming of T cells.

international immunology

Unprimed T cells are inefficiently stimulated by glycosylphosphatidylinositol-linked H-2K<sup>b</sup> because of its lipid anchor rather than defects in CD8 binding

Unprimed T cells are inefficiently stimulated by glycosylphosphatidylinositol-linked H-2Kb because of its lipid anchor rather than defects in CD8 binding

Unprimed T cells are inefficiently stimulated by glycosylphosphatidylinositol-linked H-2K^b because of its lipid anchor rather than defects in CD8 binding