ArticleThe Journal of experimental medicine1997
Altered hapten ligands antagonize trinitrophenyl-specific cytotoxic T cells and block internalization of hapten-specific receptors.
Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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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Who cites it
9 citing papers in PubMed, 49 citations in OpenAlex.
- Idiosyncratic adverse drug reactions: current concepts.Pharmacological reviews · 2013Review
- Mechanisms of cellular communication through intercellular protein transfer.Journal of cellular and molecular medicine · 2011Review
- Presentation of antagonist peptides to naive CD4+ T cells abrogates spatial reorganization of class II MHC peptide complexes on the surface of dendritic cells.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Clonal anergy induced in a CD8+ hapten-specific cytotoxic T-cell clone by an altered hapten-peptide ligand.Immunology · 2001Article
- 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
- T cell receptor (TCR) antagonism without a negative signal: evidence from T cell hybridomas expressing two independent TCRs.The Journal of experimental medicine · 1999Article
- Transient alteration of T cell fine specificity by a strong primary stimulus correlates with T cell receptor down-regulation.European journal of immunology · 1998Article
- Copresentation of natural HIV-1 agonist and antagonist ligands fails to induce the T cell receptor signaling cascade.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Understanding the mechanisms of sustained signaling and T cell activation.The Journal of experimental medicine · 1997Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low molecular chemicals (haptens) frequently cause T cell-mediated adverse immune reactions. Our previous work provided evidence that hapten-specific T cells, in analogy to those specific for nominal peptide antigens, direct their TCR towards hapten-modified, MHC-associated peptides. We now demonstrate that trinitrophenyl (TNP)-specific, class I MHC-restricted CTL from mice may exhibit exquisite specificity for subtle structural details of these hapten determinants, surpassing even the specificity of immunoglobulins. More importantly, these CTL could be antagonized by ligands altered either in their peptide sequence or in their hapten structure. The system was employed to examine the molecular basis of T cell antagonism. Whereas agonists resulted in a dose-dependent downregulation of TCR in different mouse T cell clones, antagonistic peptides totally failed to do so despite engaging the specific TCR. Moreover, simultaneous presentation of antagonist and agonist on the same antigen presenting cell prevented TCR internalization. No signs of anergy or functional receptor inactivation were observed in CTL treated with antagonist-loaded target cells. Based on a serial triggering model of T cell activation, our data favor a model in which antagonists block T cell functions by competitively engaging the specific TCR in unproductive interactions.
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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.