TNIK signaling imprints CD8+ T cell memory formation early after priming

Carla A. Jaeger-Ruckstuhl, Magdalena Hinterbrandner, Sabine Höpner, Colin E. Correnti, Ursina Lüthi, Olivier Friedli, Stefan Freigang, Mohamad F. Al Sayed, Elias D. Bührer, Michael A. Amrein, Christian M. Schürch, Ramin Radpour, Carsten Riether and Adrian F. Ochsenbein ()
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Carla A. Jaeger-Ruckstuhl: Inselspital, Bern University Hospital, University of Bern
Magdalena Hinterbrandner: Inselspital, Bern University Hospital, University of Bern
Sabine Höpner: Inselspital, Bern University Hospital, University of Bern
Colin E. Correnti: Fred Hutchinson Cancer Research Center (FHCRC)
Ursina Lüthi: Inselspital, Bern University Hospital, University of Bern
Olivier Friedli: University of Bern
Stefan Freigang: University of Bern
Mohamad F. Al Sayed: Inselspital, Bern University Hospital, University of Bern
Elias D. Bührer: Inselspital, Bern University Hospital, University of Bern
Michael A. Amrein: Inselspital, Bern University Hospital, University of Bern
Christian M. Schürch: Inselspital, Bern University Hospital, University of Bern
Ramin Radpour: Inselspital, Bern University Hospital, University of Bern
Carsten Riether: Inselspital, Bern University Hospital, University of Bern
Adrian F. Ochsenbein: Inselspital, Bern University Hospital, University of Bern

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Co-stimulatory signals, cytokines and transcription factors regulate the balance between effector and memory cell differentiation during T cell activation. Here, we analyse the role of the TRAF2-/NCK-interacting kinase (TNIK), a signaling molecule downstream of the tumor necrosis factor superfamily receptors such as CD27, in the regulation of CD8+ T cell fate during acute infection with lymphocytic choriomeningitis virus. Priming of CD8+ T cells induces a TNIK-dependent nuclear translocation of β-catenin with consecutive Wnt pathway activation. TNIK-deficiency during T cell activation results in enhanced differentiation towards effector cells, glycolysis and apoptosis. TNIK signaling enriches for memory precursors by favouring symmetric over asymmetric cell division. This enlarges the pool of memory CD8+ T cells and increases their capacity to expand after re-infection in serial re-transplantation experiments. These findings reveal that TNIK is an important regulator of effector and memory T cell differentiation and induces a population of stem cell-like memory T cells.

Date: 2020
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DOI: 10.1038/s41467-020-15413-7

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