ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Apoptotic cells activate NKT cells through T cell Ig-like mucin-like-1 resulting in airway hyperreactivity.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
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Who cites it
52 citing papers in PubMed, 74 citations in OpenAlex.
- Review
- Molecular Basis for the Differential Function of HAVCR1 Mucin Variants.Biomedicines · 2024Article
- Role of TIM-1 in the development and treatment of tumours.Frontiers in cell and developmental biology · 2024Review
- Kidney injury molecule 1 (KIM-1): a potential biomarker of acute kidney injury and tubulointerstitial injury in patients with ANCA-glomerulonephritis.Clinical kidney journal · 2023Article
- Identification of a PD-L1+Tim-1+ iNKT subset that protects against fine particulate matter-induced airway inflammation.JCI insight · 2022Article
- TIM-1 promotes proliferation and metastasis, and inhibits apoptosis, in cervical cancer through the PI3K/AKT/p53 pathway.BMC cancer · 2022Article
- The role of phosphatidylserine on the membrane in immunity and blood coagulation.Biomarker research · 2022Review
- Activating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein.Journal of innate immunity · 2022Article
- A Comprehensive Analysis of HAVCR1 as a Prognostic and Diagnostic Marker for Pan-Cancer.Frontiers in genetics · 2022Article
- lncRNA TUG1 as a ceRNA promotes PM exposure-induced airway hyper-reactivity.Journal of hazardous materials · 2021Article
- Kidney Injury Molecule 1 (KIM-1): a Multifunctional Glycoprotein and Biological Marker (Review).Sovremennye tekhnologii v meditsine · 2021Review
- The Network of Inflammatory Mechanisms in Lupus Nephritis.Frontiers in medicine · 2020Review
- Probiotics Can Boost the Antitumor Immunity of CD8Journal of immunology research · 2020Article
- Blockade of TIM-1 on the donor graft ameliorates graft-versus-host disease following hematopoietic cell transplantation.Blood advances · 2019Article
- TIM-1 serves as a receptor for Ebola virus in vivo, enhancing viremia and pathogenesis.PLoS neglected tropical diseases · 2019Article
- Understanding kidney injury molecule 1: a novel immune factor in kidney pathophysiology.American journal of translational research · 2019Review
- Fine Particulate Matter-Induced Exacerbation of Allergic Asthma via Activation of T-cell Immunoglobulin and Mucin Domain 1.Chinese medical journal · 2018Article
- TIM-1 Mediates Dystroglycan-Independent Entry of Lassa Virus.Journal of virology · 2018Article
- Anti-TIM-1 Monoclonal Antibody (RMT1-10) Attenuates Atherosclerosis By Expanding IgM-producing B1a Cells.Journal of the American Heart Association · 2018Article
- Role of CD1d- and MR1-Restricted T Cells in Asthma.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 3 countries.
Funding
Abstract
T cell Ig-like mucin-like-1 (TIM-1) is an important asthma susceptibility gene, but the immunological mechanisms by which TIM-1 functions remain uncertain. TIM-1 is also a receptor for phosphatidylserine (PtdSer), an important marker of cells undergoing programmed cell death, or apoptosis. We now demonstrate that NKT cells constitutively express TIM-1 and become activated by apoptotic cells expressing PtdSer. TIM-1 recognition of PtdSer induced NKT cell activation, proliferation, and cytokine production. Moreover, the induction of apoptosis in airway epithelial cells activated pulmonary NKT cells and unexpectedly resulted in airway hyperreactivity, a cardinal feature of asthma, in an NKT cell-dependent and TIM-1-dependent fashion. These results suggest that TIM-1 serves as a pattern recognition receptor on NKT cells that senses PtdSer on apoptotic cells as a damage-associated molecular pattern. Furthermore, these results provide evidence for a novel innate pathway that results in airway hyperreactivity and may help to explain how TIM-1 and NKT cells regulate asthma.
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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.