%0 Journal Article
%T The Glycosylphosphatidylinositol Anchor Regulates T Cell Antigen Receptor Induced IL-2 Production
%A Nathalie Vacaresse
%A Alessandra Ferzoco
%A Dominik Filipp
%A Yutaka Amemiya
%A Arun Seth
%A David Andrews
%A Taroh Kinoshita
%A Michael Julius
%J Open Journal of Immunology
%P 1-24
%@ 2162-4526
%D 2021
%I Scientific Research Publishing
%R 10.4236/oji.2021.111001
%X Differential contributions of the glycosylphosphatidylinositol (GPI)-anchor and GPI-anchored proteins (GPI-AP) to signalling remain poorly understood. Here we show that GPI-AP deficient murine clones produce on average 18 and 181-fold more IL-2 mRNA and protein, respectively, upon T cell receptor (TCR) stimulation, in a cell-intrinsic fashion. This phenotype is formally attributed to a mutation within the transferase complex that predicates the initial step in GPI-anchor biosynthesis. Conditional disruption of the transferase complex enabled the generation of primary GPI-AP deficient CD4<sup>+</sup> T cells, which produce on average 10- and 23-fold more IL-2 mRNA and protein, respectively, upon TCR stimulation. Conditional disruption of the transamidase complex yields GPI-sufficient, GPI-AP deficient primary CD4<sup>+</sup> T cells. TCR stimulation of these cells yields levels of IL-2 mRNA and protein ranging from 1 - 3 and 3-fold, respectively, of controls. These results provide the first evidence of a profound impact of GPI in the regulation of TCR signalling.
%K GPI Anchor
%K TCR Regulation
%K IL-2 Production
%U http://www.scirp.org/journal/PaperInformation.aspx?PaperID=107691