ArticlePloS one2017
The role of ADAM17 in the T-cell response against bacterial pathogens.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
13 citing papers in PubMed, 15 citations in OpenAlex.
- Characterization of the D8P1C1 Anti-ADAM17 Inhibitory Monoclonal Antibody and Generation of Its Bispecific T-Cell Engager Derivative.International journal of molecular sciences · 2026Article
- iRhom2 deficiency reduces sepsis-induced mortality associated with the attenuation of lung macrophages in mice.Histochemistry and cell biology · 2024Article
- Targeting a disintegrin and metalloprotease (ADAM) 17-CD122 axis enhances CD8Signal transduction and targeted therapy · 2024Article
- A Disintegrin and metalloproteinase carves T cell abnormalities and pathogenesis in systemic lupus erythematosus.Clinical immunology (Orlando, Fla.) · 2024Review
- The metalloprotease ADAM10 generates soluble interleukin-2 receptor alpha (sCD25) in vivo.The Journal of biological chemistry · 2022Article
- ADAM9 enhances Th17 cell differentiation and autoimmunity by activating TGF-β1.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of L-Selectin in HIV Infection.Frontiers in microbiology · 2021Review
- ADAM17, A Key Player of Cardiac Inflammation and Fibrosis in Heart Failure Development During Chronic Catecholamine Stress.Frontiers in cell and developmental biology · 2021Review
- Epigenomics and transcriptomics of systemic sclerosis CD4+ T cells reveal long-range dysregulation of key inflammatory pathways mediated by disease-associated susceptibility loci.Genome medicine · 2020Article
- A Disintegrin and Metalloproteinase-Control Elements in Infectious Diseases.Frontiers in cardiovascular medicine · 2020Review
- Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects.Frontiers in immunology · 2020Review
- ADAM17-dependent proteolysis of L-selectin promotes early clonal expansion of cytotoxic T cells.Scientific reports · 2019Article
- A unique protein kinase C-dependent pathway for tissue factor downregulation in pericytes.Journal of thrombosis and haemostasis : JTH · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors. By controlled shedding of these proteins from leukocytes, ADAM17 is able to regulate immune responses. Several ADAM17 targets on T cells have been implicated in T-cell migration, differentiation and effector functions. However, the role of ADAM17 in T-cell responses is still unclear. To characterize the function of ADAM17 in T cells, we used Adam17fl/fl×CD4cre+ mice with a T-cell restricted inactivation of the Adam17 gene. Upon stimulation, ADAM17-deficient CD4+ and CD8+ T cells were impaired in shedding of CD62L, IL-6Rα, TNF-α, TNFRI and TNFRII. Surprisingly, we could not detect profound changes in the composition of major T-cell subsets in Adam17fl/fl×CD4cre+ mice. Following infection with Listeria monocytogenes, Adam17fl/fl×CD4cre+ mice mounted regular listeria-specific CD4+ TH1 and CD8+ T-cell responses and were able to control primary and secondary infections. In conclusion, our study indicates that ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.