ArticleCellular immunology2019
In vivo administration of recombinant BTNL2-Fc fusion protein ameliorates graft-versus-host disease in mice.
Article in Cellular immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 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
- 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
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Authors and funding
7 authors.
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Abstract
Although hematopoietic stem cell transplantation (HSCT) has been widely used in the treatment of many diseases, graft-versus-host disease (GVHD) remains a major complication after allogeneic HSCT. Butyrophilin-like 2 (BTNL2) protein has been reported to have the ability to inhibit T cell proliferation in vitro; its ability to inhibit T cell responses in vivo has not been determined. We show here that in vivo administration of recombinant BTNL2-IgG2a Fc (rBTNL2-Ig) fusion protein ameliorates GVHD in mice. This is related to the ability of rBTNL2-Ig to inhibit T cell proliferation, activation and Th1/Th17 cytokine production in vivo. Furthermore, rBTNL2-Ig treatment increases the generation of regulatory T cells. Our results suggest that rBTNL2-Ig has the potential to be used in the prevention and treatment of patients with GVHD.
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Registered trials
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