ArticleThe Journal of experimental medicine1995
Dual T cell receptor alpha chain T cells in autoimmunity.
Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- Dual T cell receptor expression provides intrinsic advantage for agonist selection of thymic FoxP3+ regulatory T cells (Tregs) in the neonatal thymus.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Proportion, Function, and Generation of Dual Receptor Lymphocytes.Journal of immunology research · 2026Review
- Establishment of Autoreactive CD4International journal of molecular sciences · 2025Article
- Functional tumor-reactive CD8 + T cells in pancreatic cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Article
- scRNA+TCR-seq reveals the pivotal role of dual receptor T lymphocytes in the pathogenesis of Kawasaki disease and during IVIG treatment.Frontiers in immunology · 2024Article
- Article
- Article
- Dual TCR-α Expression on Mucosal-Associated Invariant T Cells as a Potential Confounder of TCR Interpretation.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- TCRα reporter mice reveal contribution of dual TCRα expression to T cell repertoire and function.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Molecular Mimicry and Uveitis.Frontiers in immunology · 2020Review
- Review
- TCR Retrogenic Mice as a Model To Map Self-Tolerance Mechanisms to the Cancer Mucosa Antigen GUCY2C.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- A Novel Approach of Identifying Immunodominant Self and Viral Antigen Cross-Reactive T Cells and Defining the Epitopes They Recognize.Frontiers in immunology · 2018Article
- Segmented Filamentous Bacteria Provoke Lung Autoimmunity by Inducing Gut-Lung Axis Th17 Cells Expressing Dual TCRs.Cell host & microbe · 2017Article
- Proinflammatory Dual Receptor T Cells in Chronic Graft-versus-Host Disease.Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation · 2017Article
- Cutting Edge: Dual TCRα Expression Poses an Autoimmune Hazard by Limiting Regulatory T Cell Generation.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- The highly alloreactive nature of dual TCR T cells.Current opinion in organ transplantation · 2016Review
- Unresolved issues in theories of autoimmune disease using myocarditis as a framework.Journal of theoretical biology · 2015Review
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allelic exclusion at the T cell receptor alpha locus TCR-alpha is incomplete, as demonstrated by the presence of a number of T lymphocyte clones carrying two expressed alpha chain products. Such dual alpha chain T cells have been proposed to play a role in autoimmunity, for example, because of a second TCR-alpha beta pair having bypassed negative selection by virtue of low expression. We examined this hypothesis by generating mice of various autoimmunity-prone strains carrying a hemizygous targeted disruption of the TCR-alpha locus, therefore unable to produce dual alpha chain T cells. Normal mice have a low but significant proportion of T cells expressing two cell-surface TCR-alpha chains that could be enumerated by comparison to TCR-alpha hemizygotes, which have none. Susceptibility to various autoimmune diseases was analyzed in TCR-alpha hemizygotes that had been backcrossed to disease-prone strains for several generations. The incidence of experimental allergic encephalomyelitis and of lupus is not affected by the absence of dual TCR-alpha cells. In contrast, nonobese diabetic (NOD) TCR alpha hemizygotes are significantly protected from cyclophosphamide-accelerated insulitis and diabetes. Thus, dual alpha T cells may play an important role in some but not all autoimmune diseases. Furthermore, since protected and susceptible NOD mice both show strong spontaneous responses to glutamic acid decarboxylase, responses to this antigen, if necessary for diabetetogenesis, are not sufficient.
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