ReviewSpringer seminars in immunopathology2004
TIM-1, a novel allergy and asthma susceptibility gene.
Review in Springer seminars in immunopathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 129 citations in OpenAlex.
- The potential of efferocytosis for the treatment of bronchial asthma: A review of current trends, mechanisms and prospects.Biochemistry and biophysics reports · 2025Review
- Association between vaccination, viral antibodies, and asthma prevalence in the U.S.: insights from NHANES (1999-2020).Frontiers in allergy · 2025Article
- The ability of human TIM1 to bind phosphatidylethanolamine enhances viral uptake and efferocytosis compared to rhesus and mouse orthologs.Journal of virology · 2024Article
- Chikungunya virus release is reduced by TIM-1 receptors through binding of envelope phosphatidylserine.Journal of virology · 2024Article
- The ability of human TIM1 to bind phosphatidylethanolamine enhances viral uptake and efferocytosis compared to rhesus and mouse orthologs.bioRxiv : the preprint server for biology · 2024Article
- Chikungunya Virus Release is Reduced by TIM-1 Receptors Through Binding of Envelope Phosphatidylserine.bioRxiv : the preprint server for biology · 2024Article
- Recent advances in extracellular vesicles in gastrointestinal cancer and lymphoma.Cancer science · 2023Review
- Immune checkpoint molecules in prevention and development of asthma.Frontiers in immunology · 2023Review
- TIM-1 Augments Cellular Entry of Ebola Virus Species and Mutants, Which Is Blocked by Recombinant TIM-1 Protein.Microbiology spectrum · 2022Article
- Diagnostic role of kidney injury molecule-1 in renal cell carcinoma.International urology and nephrology · 2019Review
- Regulatory functions of B cells and regulatory plasma cells.Biomedical journal · 2019Review
- Biomechanical characterization of TIM protein-mediated Ebola virus-host cell adhesion.Scientific reports · 2019Article
- Article
- TIM-1 Mediates Dystroglycan-Independent Entry of Lassa Virus.Journal of virology · 2018Article
- T-cell immunoglobulin mucin-3 expression in invasive ductal breast carcinoma: Clinicopathological correlations and association with tumor infiltration by cytotoxic lymphocytes.Molecular and clinical oncology · 2017Article
- The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation.Seminars in immunopathology · 2016Review
- Article
- Development of a Stable Cell Line, Overexpressing Human T-cell Immunoglobulin Mucin 1.Iranian journal of biotechnology · 2015Article
- KIM-1-/TIM-1-mediated phagocytosis links ATG5-/ULK1-dependent clearance of apoptotic cells to antigen presentation.The EMBO journal · 2015Article
- Interaction between TIM-1 and NPC1 Is Important for Cellular Entry of Ebola Virus.Journal of virology · 2015Article
4 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atopic diseases, including asthma, allergic rhinitis, and atopic dermatitis, are caused by environmental factors in genetically predisposed individuals. Although the prevalence of these diseases has risen dramatically over the past two decades, it has been difficult to identify the underlying causes of these diseases due to the complex interplay between the genetic and environmental factors involved. Using a congenic mouse model of asthma, we simplified this complex trait and identified the novel T cell immunoglobulin domain, mucin-like domain (TIM) gene family, that encodes transmembrane proteins expressed by CD4 T cells. Recent studies demonstrate that the TIM family, particularly TIM-1, plays a critical role in immune responses that regulate the development of atopic diseases. In humans, certain polymorphic variants of TIM-1 are strongly associated with protection against atopy, and this association occurs only in individuals who have had past infection with hepatitis A virus (HAV). Since TIM-1 functions as the cellular receptor for HAV, activation of T cells through TIM-1 by HAV or by its natural ligand may affect T cell differentiation and the development of Th2-driven allergic inflammatory responses. Epidemiologically, HAV infection is associated with a reduced risk of developing atopy, and because the incidence of HAV infection has been significantly reduced in industrialized countries over the past 30 years, the discovery of a genetic interaction between HAV and TIM-1 provides the first molecular genetic evidence for the hygiene hypothesis.
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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.