ArticleAdvanced healthcare materials2019
BTNL2-Ig Protein Attenuates Type 1 Diabetes in Non-Obese Diabetic (NOD) Mice.
Article in Advanced healthcare materials, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed.
- Emerging strategies for treating autoimmune disease with genetically modified dendritic cells.Cell communication and signaling : CCS · 2024Review
- BTNL2 promotes colitis-associated tumorigenesis in mice by regulating IL-22 production.EMBO reports · 2023Article
- Identification of TAPBPL as a novel negative regulator of T-cell function.EMBO molecular medicine · 2021Article
- Structural Insights into N-terminal IgV Domain of BTNL2, a T Cell Inhibitory Molecule, Suggests a Non-canonical Binding Interface for Its Putative Receptors.Journal of molecular biology · 2020Article
- The Role of B7 Family Molecules in Maternal-Fetal Immunity.Frontiers in immunology · 2020Review
- Accelerator or Brake: Immune Regulators in Malaria.Frontiers in cellular and infection microbiology · 2020Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Type 1 diabetes (T1D) is a T cell-mediated autoimmune disease in which insulin-producing β-cells are destroyed. Although butyrophilin-like 2 (BTNL2) has been shown to be a negative T cell regulator in vitro, its ability to inhibit T cell responses in vivo has not been determined. In this study, the effect of a recombinant BTNL2-IgG2a Fc (rBTNL2-Ig) fusion protein on T1D development in vivo is determined. It is shown here that in vivo administration of rBTNL2-Ig ameliorates T1D in non-obese diabetic (NOD) mice. This is associated with the ability of rBTNL2-Ig to inhibit the proliferation, activation, and inflammatory cytokine production from autoreactive T cells in vivo. In addition, rBTNL2-Ig treatment increases the generation of regulatory T cells. The results suggest that targeting the BTNL2 pathway has the potential to be used in the prevention and treatment of patients with T1D.
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Registered trials
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