ArticleImmunity2013
T cell-derived protein S engages TAM receptor signaling in dendritic cells to control the magnitude of the immune response.
Article in Immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 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.
The trial behind it
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
123 citing papers in PubMed, 181 citations in OpenAlex.
- Analysis of receptor tyrosine kinase genetics identifies two novel risk loci in GAS6 and PROS1 in Behçet's disease.Scientific reports · 2016Trial
- Fc-Dependent Targeting of the GAS6-MERTK Axis With Monoclonal and Bispecific Antibodies Overcomes Drug Resistance Across EGFR Mutations in Exons 19, 20, and 21.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Recent advances in TMEM16F: structural plasticity, functional versatility, and implications for human diseases.Cell communication and signaling : CCS · 2026Review
- Article
- DIA-based serum proteomics of the complement-coagulation cascade identifies candidate biomarkers for myasthenia gravis.Frontiers in neuroscience · 2026Article
- Pregnancy-associated metabolic adaptations in circulating monocytes and macrophages favor clearance functions.Frontiers in immunology · 2026Article
- MERTK inhibition improves therapeutic efficacy of immune checkpoint inhibitors in hepatocellular carcinoma.Oncoimmunology · 2025Article
- ProS1-MerTK signaling in CD4 T cells: implications for TIL expansion and functionality.Oncoimmunology · 2025Article
- Phospholipid scramblases TMEM16F and Xkr8 mediate distinct features of phosphatidylserine (PS) externalization and immune suppression to promote tumor growth.Cell death discovery · 2025Article
- Tyro3 deletion is protective in experimental autoimmune encephalomyelitis.Immunology and cell biology · 2025Article
- RNA Sequencing Reveals Inflammatory and Metabolic Changes in the Lung and Brain After Carbon Black and Naphthalene Whole Body Inhalation Exposure in a Rodent Model of Military Burn Pit Exposures.International journal of molecular sciences · 2025Article
- Recent advances in TAM mechanisms in lung diseases.Journal of translational medicine · 2025Review
- Navigating TAM receptor dynamics in tumour immunotherapy.Cancer immunology, immunotherapy : CII · 2025Review
- Dys-regulated phosphatidylserine externalization as a cell intrinsic immune escape mechanism in cancer.Cell communication and signaling : CCS · 2025Review
- Mertk signaling and immune regulation in T cells.Journal of leukocyte biology · 2024Article
- MERTK inhibition selectively activates a DC - T-cell axis to provide anti-leukemia immunity.Leukemia · 2024Article
- Functions of TAM Receptors and Ligands Protein S and Gas6 in Atherosclerosis and Cardiovascular Disease.International journal of molecular sciences · 2024Review
- MerTK Induces Dysfunctional Dendritic Cells by Metabolic Reprogramming.Cancer immunology research · 2024Article
- The amalgam of naive CD4Immunity · 2024Article
- In the Eyes of the Beholder-NewInternational journal of molecular sciences · 2024Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 1 country.
Funding
Abstract
Dendritic cell (DC) activation is essential for the induction of immune defense against pathogens, yet needs to be tightly controlled to avoid chronic inflammation and exaggerated immune responses. Here, we identify a mechanism of immune homeostasis by which adaptive immunity, once triggered, tempers DC activation and prevents overreactive immune responses. T cells, once activated, produced Protein S (Pros1) that signaled through TAM receptor tyrosine kinases in DCs to limit the magnitude of DC activation. Genetic ablation of Pros1 in mouse T cells led to increased expression of costimulatory molecules and cytokines in DCs and enhanced immune responses to T cell-dependent antigens, as well as increased colitis. Additionally, PROS1 was expressed in activated human T cells, and its ability to regulate DC activation was conserved. Our results identify a heretofore unrecognized, homeostatic negative feedback mechanism at the interface of adaptive and innate immunity that maintains the physiological magnitude of the immune response.
Indexed as
Identifiers
What OpenQuestion holds
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.