ArticleProceedings of the National Academy of Sciences of the United States of America1998
Copresentation of natural HIV-1 agonist and antagonist ligands fails to induce the T cell receptor signaling cascade.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
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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
13 citing papers in PubMed, 44 citations in OpenAlex.
- Dual Molecular Mechanisms Govern Escape at Immunodominant HLA A2-Restricted HIV Epitope.Frontiers in immunology · 2017Article
- On Peptides and Altered Peptide Ligands: From Origin, Mode of Action and Design to Clinical Application (Immunotherapy).International archives of allergy and immunology · 2016Review
- Dissecting the dynamics of HIV-1 protein sequence diversity.PloS one · 2013Article
- T cell recognition of weak ligands: roles of signaling, receptor number, and affinity.Immunologic research · 2011Review
- Peptide antagonism as a mechanism for NK cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- A unique unresponsive CD4+ T cell phenotype post TCR antagonism.Cellular immunology · 2010Article
- Availability of a diversely avid CD8+ T cell repertoire specific for the subdominant HLA-A2-restricted HIV-1 Gag p2419-27 epitope.Journal of immunology (Baltimore, Md. : 1950) · 2007Article
- Enhanced immunogenicity of CTL antigens through mutation of the CD8 binding MHC class I invariant region.European journal of immunology · 2007Article
- De novo generation of escape variant-specific CD8+ T-cell responses following cytotoxic T-lymphocyte escape in chronic human immunodeficiency virus type 1 infection.Journal of virology · 2005Article
- T cell receptor antagonism interferes with MHC clustering and integrin patterning during immunological synapse formation.The Journal of cell biology · 2004Article
- T-cell receptor-mediated anergy of a human immunodeficiency virus (HIV) gp120-specific CD4(+) cytotoxic T-cell clone, induced by a natural HIV type 1 variant peptide.Journal of virology · 2000Article
- Immunological self/nonself discrimination: integration of self vs nonself during cognate T cell interactions with antigen-presenting cells.Immunologic research · 1999Review
- HIV-1 variation diminishes CD4 T lymphocyte recognition.The Journal of experimental medicine · 1998Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
It is not known how human immunodeficiency virus type 1 (HIV-1)-derived antagonist peptides interfere with intracellular activation of cytotoxic T lymphocytes (CTL). We identified Gag epitope variants in HIV-1-infected patients that act as antagonists of CTL responses to unmutated epitopes. We then investigated the effect that presentation of each variant has on the early events of T cell receptor (TCR) signal transduction. We found that altered peptide ligands (APL) failed to induce phosphorylation of pp36, a crucial adaptor protein involved in TCR signal transduction. We further investigated the effect that simultaneous presentation of APL and native antigen at low, physiological, peptide concentrations (1 nM) has on TCR signal transduction, and we found that the presence of APL can completely inhibit induction of the protein tyrosine phosphorylation events of the TCR signal transduction cascade.
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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.