Ferguson, M.A.J., Hart, G.W. and Kinoshita, T. (2017) Chapter 12. Glycosylphosphatidylinositol Anchors. In: Rd, Varki, A., Cummings, R.D., Esko, J.D., Stanley, P., Hart, G.W., Aebi, M., Darvill, A.G., Kinoshita, T., Packer, N.H., Prestegard, J.H., Schnaar, R.L. and Seeberger, P.H., Eds., Essentials of Glycobiology, Cold Spring Harbor, New York, 137-150.

has been cited by the following article:

• TITLE: The Glycosylphosphatidylinositol Anchor Regulates T Cell Antigen Receptor Induced IL-2 Production

  AUTHORS: Nathalie Vacaresse, Alessandra Ferzoco, Dominik Filipp, Yutaka Amemiya, Arun Seth, David Andrews, Taroh Kinoshita, Michael Julius

  KEYWORDS: GPI Anchor, TCR Regulation, IL-2 Production

  JOURNAL NAME: Open Journal of Immunology, Vol.11 No.1, March 12, 2021

  ABSTRACT: 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+ 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+ 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.