Journal article

PTPN2 Deficiency Enhances Programmed T Cell Expansion and Survival Capacity of Activated T Cells

M Flosbach, SG Oberle, S Scherer, J Zecha, M von Hoesslin, F Wiede, V Chennupati, JG Cullen, M List, JK Pauling, J Baumbach, B Kuster, T Tiganis, D Zehn

Cell Reports | CELL PRESS | Published : 2020

Abstract

Manipulating PTPN2 has potential for advancing immunotherapies. However, it is unclear how PTPN2 impacts the activation, survival, and memory formation of T cells. Flosbach et al. demonstrate that PTPN2-deficient T cells are less dependent on cytokines and show increased programmed expansion, and short-lived effector T cells have enhanced survival and expansion capacity.

University of Melbourne Researchers

Grants

Awarded by Swiss Vaccine Research Institute


Funding Acknowledgements

We thank M. Prlic for input, feedback, and suggestions; B. Dotterbock, W. Schmid, and C. Amette for technical assistance; and S. Schleicher and C. Lechner for animal husbandry. MEC.B7.SigOVA cells were kindly provided by S. Schoenberger (San Diego, CA, USA). Work in the D.Z. laboratory was supported by a European Research Council starting grant (ProtecTC) and subsequently by a European Research Council consolidator grant (ToCCaTa), by grants from the Swiss National Science Foundation (SNSF; CRSII3_160708, 310030E-16187, 51PHP0_157319, and PP00P3_144883) and the Swiss Vaccine Research Institute (SVRI), and by grants from the German Research Foundation (SFB1054 and SFB1371). Contributions by J.K.P. were funded by the Bavarian State Ministry of Science and the Arts in the framework of the Bavarian Research Institute for Digital Transformation (BIDT). Work in the T.T. laboratory is supported by the National Health and Medical Research Council (NHMRC) of Australia; T.T. is an NHMRC Principal Research Fellow. J.B. is grateful for financial support from the H2020 project RepoTrial (777111), Federal Ministry of Education and Research (BMBF) project CLINSPECT-M (grant 031 L0214A), and grants from the German Research Foundation (SFB1371). The work from J.Z. and B.K. was supported by the German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ).