Journal
CANCER CELL
Volume 36, Issue 3, Pages 268-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2019.07.008
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Funding
- Fondation ARC pour la Recherche sur le Cancer
- 'Agence Nationale de la Recherche' (Labex SIGNALIFE) [ANR-11-LABX-0028-01]
- Canceropole PACA
- Institut National Du Cancer (INCA)
- Conseil Regional PACA
- French Ministry of Research
- la Fondation pour la Recherche Medicale (FRM)
- Aides individuelles aux jeunes chercheur ville de Nice
- Commissariat aux Grands Investissements [ANR-10-INBS-09-03, ANR-10-INBS-09-02]
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GAPDH is emerging as a key player in T cell development and function. To investigate the role of GAPDH in T cells, we generated a transgenic mouse model overexpressing GAPDH in the T cell lineage. Aged mice developed a peripheral Tfh-like lymphoma that recapitulated key molecular, pathological, and immunophenotypic features of human angioimmunoblastic T cell lymphoma (AITL). GAPDH induced non-canonical NF-kappa B pathway activation in mouse T cells, which was strongly activated in human AITL. We developed a NIK inhibitor to reveal that targeting the NF-kappa B pathway prolonged AITL-bearing mouse survival alone and in combination with anti-PD-1. These findings suggest the therapeutic potential of targeting NF-kappa B signaling in AITL and provide a model for future AITL therapeutic investigations.
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