ArticleJournal of immunology (Baltimore, Md. : 1950)2013
The B7-independent isoform of CTLA-4 functions to regulate autoimmune diabetes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Regulation of Treg cells by cytokine signaling and co-stimulatory molecules.Frontiers in immunology · 2024Review
- Spontaneous immunological activities in the target tissue of vitiligo-prone Smyth and vitiligo-susceptible Brown lines of chicken.Frontiers in immunology · 2024Article
- Current Understanding of Cytotoxic T Lymphocyte Antigen-4 (CTLA-4) Signaling in T-Cell Biology and Disease Therapy.Molecules and cells · 2022Review
- In Vivo Induction of Regulatory T Cells Via CTLA-4 Signaling Peptide to Control Autoimmune Encephalomyelitis and Prevent Disease Relapse.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- The yin and yang of co-inhibitory receptors: toward anti-tumor immunity without autoimmunity.Cell research · 2020Review
- Type 1 diabetes pathogenesis and the role of inhibitory receptors in islet tolerance.Annals of the New York Academy of Sciences · 2020Review
- Time to dissect the autoimmune etiology of cancer antibody immunotherapy.The Journal of clinical investigation · 2020Review
- CD19+IgM+ cells demonstrate enhanced therapeutic efficacy in type 1 diabetes mellitus.JCI insight · 2018Article
- Regulation of human T cell responses by dNP2-ctCTLA-4 inhibits human skin and microvessel graft rejection.Biomaterials · 2018Article
- Dichotomous roles of co-stimulatory molecules in diabetes mellitus.Oncotarget · 2018Review
- Co-stimulatory and Co-inhibitory Pathways in Autoimmunity.Immunity · 2016Review
- Podocyte Expression of B7-1/CD80: Is it a Reliable Biomarker for the Treatment of Proteinuric Kidney Diseases with Abatacept?Journal of the American Society of Nephrology : JASN · 2016Article
- Clinical intraocular islet transplantation is not a number issue.CellR4-- repair, replacement, regeneration, & reprogramming · 2016Article
- Article
- Prediction and prevention of type 1 diabetes: update on success of prediction and struggles at prevention.Pediatric diabetes · 2015Review
- dNP2 is a blood-brain barrier-permeable peptide enabling ctCTLA-4 protein delivery to ameliorate experimental autoimmune encephalomyelitis.Nature communications · 2015Article
- A transendocytosis model of CTLA-4 function predicts its suppressive behavior on regulatory T cells.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Opposing effects of CTLA4 insufficiency on regulatory versus conventional T cells in autoimmunity converge on effector memory in target tissue.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- T-cell costimulation protects obesity-induced adipose inflammation and insulin resistance.Diabetes · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The critical role of CTLA-4 in inhibiting Ag-driven T cell responses upon engagement with its ligands, B7-1 and B7-2 and its importance for peripheral T cell tolerance and T cell homeostasis has been studied intensively. The CTLA-4 splice variant ligand-independent (li)-CTLA-4 is expressed in naive and activated T cells and can actively alter T cell signaling despite its lack of a B7 binding domain. To study the effect of li-CTLA-4 in regulating T cell responses in the context of autoimmunity, we engineered a B6.CTLA-4 (floxed-Exon2)-BAC-transgene, resulting in selective expression of li-CTLA-4 upon Cre-mediated deletion of Exon 2. Introducing the B6.BAC into the NOD background, which is genetically deficient for li-CTLA-4, restores mRNA levels of li-CTLA-4 to those observed in C57BL/6 mice. Furthermore, re-expressing this ligand nonbinding isoform in NOD mice reduced IFN-γ production in T effector cells accompanied by a significant decrease in insulitis and type 1 diabetes frequency. However, selective expression of li-CTLA-4 could not fully rescue the CTLA-4 knockout disease phenotype when bred onto NOD.BDC2.5.CTLA-4 knockout background because of the requirement of the full-length, B7-binding CTLA-4 molecule on T effector cells. Thus, the li-CTLA-4 form, when expressed at physiologic levels in the CTLA-4-sufficient NOD background can suppress autoimmunity; however, the functionality of the li-CTLA-4 isoform depends on the presence of the full-length molecule to alter effector T cell signaling.
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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.