ArticlePloS one2017
Directed evolution of a soluble human DR3 receptor for the inhibition of TL1A induced cytokine secretion.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Unravelling the TL1A-DR3 axis in Hidradenitis suppurativa.Frontiers in immunology · 2026Review
- Joint Microbiota Suggests Articular Dysbiosis in Experimental Murine Spondyloarthritis and Histological Detection of Bacteria in Human SpA Joints.International journal of inflammation · 2025Article
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- TNF-like ligand 1A is associated with progression and prognosis of human gastric cancer.OncoTargets and therapy · 2019Article
- Directed evolution of SIRT6 for improved deacylation and glucose homeostasis maintenance.Scientific reports · 2018Article
- Article
- Increased Potency of a Bi-specific TL1A-ADAM17 (TACE) Inhibitor by Cell Surface Targeting.Frontiers in molecular biosciences · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF-like 1A (TL1A) is a cytokine belonging to the TNF superfamily that promotes inflammation in autoimmune diseases. Inhibiting the interaction of TL1A with the endogenous death-domain receptor 3 (DR3) offers a therapeutic approach for treating TL1A-induced autoimmune diseases. Here, we generated improved DR3 variants showing increased TL1A binding affinity and stability using a directed evolution approach. Given the high cysteine content and post-translational modification of DR3, we employed yeast surface display and expression in mammalian cell lines for screening, expression and characterization of improved DR3 variants. A cell-based assay performed with the human TF-1 cell line and CD4+ T cells showed that two improved DR3 mutants efficiently inhibited TL1A-induced cell death and secretion of IFN-γ, respectively. These DR3 mutants can be used as drug candidates for the treatment of inflammatory bowel diseases and for other autoimmune diseases, including rheumatic arthritis and asthma.
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Registered trials
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