ArticleImmunology2004
Major histocompatibility complex class I-intercellular adhesion molecule-1 association on the surface of target cells: implications for antigen presentation to cytotoxic T lymphocytes.
Article in Immunology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 31 citations in OpenAlex.
- Risperidone reduces individualized morphometric similarity deviation in schizophrenia and associates with cortical transcriptomic patterns.Schizophrenia (Heidelberg, Germany) · 2026Article
- The role of peptide conformation presented by MHC in the induction of TCR triggering.Biophysical journal · 2025Article
- Homotypic and heterotypicCurrent research in immunology · 2022Review
- Open MHC Class I Conformers: A Look through the Looking Glass.International journal of molecular sciences · 2021Review
- Related parameters of affinity and stability prediction of HLA-A*2402 restricted antigen peptides based on molecular docking.Annals of translational medicine · 2021Article
- Extent of MHC Clustering Regulates Selectivity and Effectiveness of T Cell Responses.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- MICAL-L1-related and unrelated mechanisms underlying elongated tubular endosomal network (ETEN) in human dendritic cells.Communicative & integrative biology · 2014Article
- Core-based lipid nanoparticles as a nanoplatform for delivery of near-infrared fluorescent imaging agents.American journal of nuclear medicine and molecular imaging · 2014Article
- Immunosuppressive drug therapy.Cold Spring Harbor perspectives in medicine · 2013Review
- Evidence that the density of self peptide-MHC ligands regulates T-cell receptor signaling.PloS one · 2012Article
- Mechanisms controlling granule-mediated cytolytic activity of cytotoxic T lymphocytes.Immunologic research · 2011Review
- Can oligomeric T-cell receptor be used as a tool to detect viral peptide epitopes on infected cells?Clinical immunology (Orlando, Fla.) · 2009Article
- Increased mobility of major histocompatibility complex I-peptide complexes decreases the sensitivity of antigen recognition.The Journal of biological chemistry · 2008Article
- Varicella-zoster virus modulates NF-kappaB recruitment on selected cellular promoters.Journal of virology · 2007Article
- Quantum dot/peptide-MHC biosensors reveal strong CD8-dependent cooperation between self and viral antigens that augment the T cell response.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Polarization and segregation of the T-cell receptor (TCR) and integrins upon productive cytotoxic T-lymphocyte (CTL) target cell encounters are well documented. Much less is known about the redistribution of major histocompatibility complex class I (MHC-I) and intercellular adhesion molecule-1 (ICAM-1) proteins on target cells interacting with CTLs. Here we show that human leucocyte antigen-A2 (HLA-A2) MHC-I and ICAM-1 are physically associated and recovered from both the raft fraction and the fraction of soluble membranes of target cells. Conjugation of target cells with surrogate CTLs, i.e. polystyrene beads loaded with antibodies specific for HLA-A2 and ICAM-1, induced the accumulation of membrane rafts, and beads loaded with ICAM-1-specific antibodies caused the selective recruitment of HLA-A2 MHC-I at the contact area of the target cells. Disruption of raft integrity on target cells led to a release of HLA-A2 and ICAM-1 from the raft fraction, abatement of HLA-A2 polarization, and diminished the ability of target cells bearing viral peptides to induce a Ca(2+) flux in virus-specific CTLs. These data suggest that productive engagement of ICAM-1 on target cells facilitates the polarization of MHC-I at the CTL-target cell interface, augmenting presentation of cognate peptide-MHC (pMHC) complexes to CTLs. We propose that ICAM-1-MHC-I association on the cell membrane is a mechanism that enhances the linkage between antigen recognition and early immunological synapse formation.
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.