ArticleOncotarget2016
TIM-4 is expressed on invariant NKT cells but dispensable for their development and function.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 11 citations in OpenAlex.
- Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- IRG1/itaconate enhances efferocytosis by activating Nrf2-TIM4 signaling pathway to alleviate con A induced autoimmune liver injury.Cell communication and signaling : CCS · 2025Article
- Tim-4 alleviates acute hepatic injury by modulating homeostasis and function of NKT cells.Clinical and experimental immunology · 2024Article
- TIM-4 increases the proportion of CD4Cancer medicine · 2024Article
- Function and characteristics of TIM‑4 in immune regulation and disease (Review).International journal of molecular medicine · 2023Review
- RecipientFrontiers in transplantation · 2023Article
- The role of phosphatidylserine on the membrane in immunity and blood coagulation.Biomarker research · 2022Review
- Tim-4 in Health and Disease: Friend or Foe?Frontiers in immunology · 2020Review
- The ins and outs of type I iNKT cell development.Molecular immunology · 2019Review
- Mixed Signals: Co-Stimulation in Invariant Natural Killer T Cell-Mediated Cancer Immunotherapy.Frontiers in immunology · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
T cell immunoglobulin and mucin-4 (TIM-4), mainly expressed on antigen presenting cells, plays a versatile role in immunoregulation. CD1d-restricted invariant natural killer T (iNKT) cells are potent cells involved in the diverse immune responses. It was recently reported that recombinant TIM-4 (rTIM-4) alone enhanced cytokine production in NKT hybridoma, DN32.D3 cells. Hence, we hypothesized that TIM-4 might regulate iNKT cell biology, especially their function of cytokine secretion. For the first time, we identified that TIM-4 was expressed in thymus iNKT cells, and its expression increased upon iNKT cell migration to the secondary lymphoid organs, especially in lymph nodes. Using TIM-4-deficient mice, we found that lack of TIM-4 did not disturb iNKT cell development, maturation, peripheral homeostasis and cytokine secretion. Moreover, TIM-4 deficiency did not alter the polarization of iNKT sublineages, including NKT1, NKT2 and NKT17. Finally, the mixed bone marrow transfer experiments further confirmed normal iNKT cell development and function from TIM-4-deficient bone marrow. In conclusion, our data suggest that TIM-4 is expressed on iNKT cells but dispensable for their development and function.
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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.