ArticleProceedings of the National Academy of Sciences of the United States of America1998
Disruption of the CD4-major histocompatibility complex class II interaction blocks the development of CD4(+) T cells in vivo.
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 16 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
16 citing papers in PubMed.
- The current landscape of CAR T-cell therapy for solid tumors: Mechanisms, research progress, challenges, and counterstrategies.Frontiers in immunology · 2023Review
- Negative Regulation of Zap70 by Lck Forms the Mechanistic Basis of Differential Expression in CD4 and CD8 T Cells.Frontiers in immunology · 2022Article
- The expansion of targetable biomarkers for CAR T cell therapy.Journal of experimental & clinical cancer research : CR · 2018Review
- CD83 increases MHC II and CD86 on dendritic cells by opposing IL-10-driven MARCH1-mediated ubiquitination and degradation.The Journal of experimental medicine · 2011Article
- The activation threshold of CD4+ T cells is defined by TCR/peptide-MHC class II interactions in the thymic medulla.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Restricted autoantigen recognition associated with deletional and adaptive regulatory mechanisms.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- An MHC class II restriction bias in CD4 T cell responses toward I-A is altered to I-E in DM-deficient mice.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- The spectrum of HLA-DQ and HLA-DR alleles, 2006: a listing correlating sequence and structure with function.Immunogenetics · 2007Article
- Restricted MHC-peptide repertoire predisposes to autoimmunity.The Journal of experimental medicine · 2005Article
- Coevolution of TCR-MHC interactions: conserved MHC tertiary structure is not sufficient for interactions with the TCR.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- An antagonist peptide mediates positive selection and CD4 lineage commitment of MHC class II-restricted T cells in the absence of CD4.The Journal of experimental medicine · 2005Article
- The role of CD4 in regulating homeostasis of T helper cells.Immunologic research · 2002Review
- Influence of CD4 T cells and the source of major histocompatibility complex class II-restricted peptides on cytotoxic T-cell priming by dendritic cells.Immunology · 2002Article
- Paradoxical intrathymic positive selection in mice with only a covalently presented agonist peptide.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Insights into T-cell development from studies using transgenic and knockout mice.Molecular biotechnology · 2001Review
- Cognate stimulatory B-cell-T-cell interactions are critical for T-cell help recruited by glycoconjugate vaccines.Infection and immunity · 1999Article
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.
Funding
Abstract
The experiments presented in this report were designed to specifically examine the role of CD4-major histocompatibility complex (MHC) class II interactions during T cell development in vivo. We have generated transgenic mice expressing class II molecules that cannot interact with CD4 but that are otherwise competent to present peptides to the T cell receptor. MHC class II expression was reconstituted in Abeta gene knock-out mice by injection of a transgenic construct encoding either the wild-type I-Abetab protein or a construct encoding a mutation designed to specifically disrupt binding to the CD4 molecule. We demonstrate that the mutation, EA137 and VA142 in the beta2 domain of I-Ab, is sufficient to disrupt CD4-MHC class II interactions in vivo. Furthermore, we show that this interaction is critical for the efficient selection of a complete repertoire of mature CD4(+) T helper cells as evidenced by drastically reduced numbers of conventional CD4(+) T cells in animals expressing the EA137/VA142 mutant I-Ab and by the failure to positively select the transgenic AND T cell receptor on the mutated I-Ab. These results underscore the importance of the CD4-class II interaction in the development of mature peripheral CD4(+) T cells.
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.