ArticleEuropean journal of immunology2011
Th17 differentiation is the default program for DPP2-deficient T-cell differentiation.
Article in European journal of immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- The Role of Dipeptidyl Peptidase Inhibitors in Pulmonary Diseases.Biomedicines · 2026Review
- DPP2/7 is a Potential Predictor of Prognosis and Target in Immunotherapy in Colorectal Cancer: An Integrative Multi-omics Analysis.Combinatorial chemistry & high throughput screening · 2024Article
- Unravelling the immunological roles of dipeptidyl peptidase 4 (DPP4) activity and/or structure homologue (DASH) proteins.Clinical and experimental immunology · 2016Review
- Divergence in gene expression within and between two closely related flycatcher species.Molecular ecology · 2016Article
- The Dipeptidyl Peptidase Family, Prolyl Oligopeptidase, and Prolyl Carboxypeptidase in the Immune System and Inflammatory Disease, Including Atherosclerosis.Frontiers in immunology · 2015Review
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Dipeptidyl peptidase 2 (DPP2) is an N-terminal dipeptidase, required for maintaining lymphocytes in a resting state. Mutant mice with T-cell-specific knock-down (kd) of DPP2 (lck-DPP2 kd) were generated and analyzed for their phenotype. Normal thymocyte development and a modest increase in the proportions of peripheral T cells were observed in these mice compared with littermate controls. Interestingly, the peripheral T cells were hyperactive upon TCR stimulation in vitro, although they did not express any activation markers. Furthermore, CD3-crosslinking in the naïve CD4(+) and CD8(+) T cells of lck-DPP2 kd mice resulted mainly in IL-17 production. Similarly, the mutant T cells secreted primarily IL-17 after in vivo priming and in vitro antigen-specific restimulation. These data suggest that IL-17 production is the default program for T-cell differentiation in the absence of DPP2. Thus, DPP2 seems to impose a threshold for quiescent T cells, preventing them from drifting into cell cycle.
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Registered trials
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