ArticleThe Journal of clinical investigation2014
Fragile TIM-4-expressing tissue resident macrophages are migratory and immunoregulatory.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- Research on tissue-resident macrophages in the field of cancer research: a bibliometric analysis from 2004 to 2025.Cell adhesion & migration · 2026Review
- Infiltration of TIM4-positive intratumoral macrophages serves as an adverse prognostic factor in breast cancer.Breast cancer (Tokyo, Japan) · 2026Article
- Suppression of cardiac allograft vasculopathy by a macrophage efferocytosis receptor.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2026Article
- Efferocytosis: The Silent Guardian of Tissue Homeostasis and Cardiovascular Health.Journal of cardiovascular development and disease · 2025Review
- B7 Family Molecule VSIG4 Regulates Pulmonary Anti-Influenza Immune Responses via C-Type Lectin Signal Pathway.Vaccines · 2025Article
- Cardiac macrophage: Insights from murine models to translational potential for human studies.Journal of molecular and cellular cardiology · 2025Review
- Retention of ES cell-derived 129S genome drives NLRP1 hypersensitivity and transcriptional deregulation in Nlrp3Cell death and differentiation · 2024Article
- CD169International journal of molecular sciences · 2024Article
- Modulating Lipid-Polymer Nanoparticles' Physicochemical Properties to Alter Macrophage Uptake.ACS biomaterials science & engineering · 2024Article
- TIM proteins and microRNAs: distinct impact and promising interactions on transplantation immunity.Frontiers in immunology · 2024Review
- Article
- Single-nucleus RNA sequencing reveals heterogeneity among multiple white adipose tissue depots.Life metabolism · 2023Article
- Macrophages in cardiac remodelling after myocardial infarction.Nature reviews. Cardiology · 2023Review
- Multiple Shades of Gray-Macrophages in Acute Allograft Rejection.International journal of molecular sciences · 2023Review
- 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 efferocytosis in neuro-degenerative diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- A Microbiota-Dependent Subset of Skin Macrophages Protects Against Cutaneous Bacterial Infection.Frontiers in immunology · 2022Article
- The Evolving Roles of Cardiac Macrophages in Homeostasis, Regeneration, and Repair.International journal of molecular sciences · 2021Review
- Innovative Systems to Deliver Allergen Powder for Epicutaneous Immunotherapy.Frontiers in immunology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Macrophages characterized as M2 and M2-like regulate immune responses associated with immune suppression and healing; however, the relationship of this macrophage subset to CD169+ tissue-resident macrophages and their contribution to shaping alloimmune responses is unknown. Here we identified a population of M2-like tissue-resident macrophages that express high levels of the phosphatidylserine receptor TIM-4 and CD169 (TIM-4hiCD169+). Labeling and tracking of TIM-4hiCD169+ macrophages in mice revealed that this population is a major subset of tissue-resident macrophages, homes to draining LNs following oxidative stress, exhibits an immunoregulatory and hypostimulatory phenotype that is maintained after migration to secondary lymphoid organs, favors preferential induction of antigen-stimulated Tregs, and is highly susceptible to apoptosis. Moreover, CD169+ tissue-resident macrophages were resistant to oxidative stress-induced apoptosis in mice lacking TIM-4. Compared with heart allografts from WT mice, Tim4-/- heart allografts survived much longer and were more easily tolerized by non-immunosuppressed recipients. Furthermore, Tim4-/- allograft survival was associated with the infiltration of Tregs into the graft. Together, our data provide evidence that M2-like TIM-4hiCD169+ tissue-resident macrophages are immunoregulatory and promote engraftment of cardiac allografts, but their influence is diminished by TIM-4-dependent programmed cell death.
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.