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Latchman, Y., Wood, C.R., Chernova, T., Chaudhary, D., Borde, M., Chernova, I., Iwai, Y., Long, A.J., Brown, J.A., Nunes, R., Greenfield, E.A., Bourque, K., Boussiotis, V.A., Carter, L.L., Carreno, B.M., Malenkovich, N., Nishimura, H., Okazaki, T., Honjo, T., Sharpe, A.H. and Freeman, G.J. (2001) PD-L2 Is a Second Ligand for PD-1 and Inhibits T Cell Activation. Nature Immunology, 2, 261-268.
https://doi.org/10.1038/85330

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.