ArticleJournal of autoimmunity2010
A recombinant heavy chain antibody approach blocks ART2 mediated deletion of an iNKT cell population that upon activation inhibits autoimmune diabetes.
Article in Journal of autoimmunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Administration of an AAV vector coding for a P2X7-blocking nanobody-based biologic ameliorates colitis in mice.Journal of nanobiotechnology · 2024Article
- Tumour immune escape via P2X7 receptor signalling.Frontiers in immunology · 2023Review
- P2X7 receptor as the regulator of T-cell function in intestinal barrier disruption.World journal of gastroenterology · 2022Review
- Evaluation of nanobody-based biologics targeting purinergic checkpoints in tumor modelsFrontiers in immunology · 2022Article
- CD70 Inversely Regulates Regulatory T Cells and Invariant NKT Cells and Modulates Type 1 Diabetes in NOD Mice.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- P2X7 Receptor at the Crossroads of T Cell Fate.International journal of molecular sciences · 2020Review
- The Role of CD38 on the Function of Regulatory B Cells in a Murine Model of Lupus.International journal of molecular sciences · 2018Article
- CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism.Scientific reports · 2018Article
- Perspectives for the Development of CD38-Specific Heavy Chain Antibodies as Therapeutics for Multiple Myeloma.Frontiers in immunology · 2018Review
- Nanobody-Based Biologics for Modulating Purinergic Signaling in Inflammation and Immunity.Frontiers in pharmacology · 2018Review
- Interferon-γ Limits Diabetogenic CD8Diabetes · 2017Article
- The Presence and Preferential Activation of Regulatory T Cells Diminish Adoptive Transfer of Autoimmune Diabetes by Polyclonal Nonobese Diabetic (NOD) T Cell Effectors into NSG versus NOD-scid Mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- P2X7 on Mouse T Cells: One Channel, Many Functions.Frontiers in immunology · 2015Review
- Mouse Invariant Monoclonal Antibody NKT14: A Novel Tool to Manipulate iNKT Cell Function In Vivo.PloS one · 2015Article
- Nanobodies as modulators of inflammation: potential applications for acute brain injury.Frontiers in cellular neuroscience · 2014Article
- Calcium insufficiency accelerates type 1 diabetes in vitamin D receptor-deficient nonobese diabetic (NOD) mice.Endocrinology · 2011Article
- ADP-ribosylation of arginine.Amino acids · 2011Review
- Testing the role of P2X7 receptors in the development of type 1 diabetes in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Extracellular NAD+ shapes the Foxp3+ regulatory T cell compartment through the ART2-P2X7 pathway.The Journal of experimental medicine · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The ectoenzyme ADP-ribosyltransferase 2.2 (ART2.2) can apoptotically delete various T-cell subsets. Depending on the involved apoptotic T-cell subset, enhanced ART2.2 activity could result in immunosuppression or autoimmunity. Diminished activity of the CD38 ectoenzyme that normally represents a counter-regulatory competitor for the NAD substrate represents one mechanism enhancing ART2.2 activity. Hence, it would be desirable to develop an agent that efficiently blocks ART2.2 activity in vivo. While the llama derived recombinant s+16 single domain antibody overcame the difficulty of specifically targeting the ART2.2 catalytic site potential therapeutic use of this reagent is limited due to short in vivo persistence. Thus, we tested if a modified version of s+16 incorporating the murine IgG1 Fc tail (s+16Fc) mediated long-term efficient in vivo suppression of ART2.2. We reasoned an ideal model to test the s+16Fc reagent were NOD mice in which genetic ablation of CD38 results in an ART2.2 mediated reduction in already sub-normal numbers of immunoregulatory natural killer T-(NKT) cells to a level that no longer allows them when activated by the super-agonist alpha-galactosylceramide (alpha-GalCer) to elicit effects inhibiting autoimmune type 1 diabetes (T1D) development. Treatment with s+16Fc efficiently mediated long-term in vivo inhibition of ART2.2 activity in NOD.CD38(null) mice, restoring their iNKT cell numbers to levels that upon alpha-GalCer activation were capable of inhibiting T1D development.
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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.