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Hochsmann, B., Murakami, Y., Osato, M., Knaus, A., Kawamoto, M., Inoue, N., Hirata, T., Murata, S., Anliker, M., Eggermann, T., Jager, M., Floettmann, R., Hollein, A., Murase, S., Ueda, Y., Nishimura, J.I., Kanakura, Y., Kohara, N., Schrezenmeier, H., Krawitz, P.M. and Kinoshita, T. (2019) Complement and Inflammasome Overactivation Mediates Paroxysmal Nocturnal Hemoglobinuria with Autoinflammation. Journal of Clinical Investigation, 129, 5123-5136.
https://doi.org/10.1172/JCI123501

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.