ArticleProceedings of the National Academy of Sciences of the United States of America2022
Biosensors for inflammation as a strategy to engineer regulatory T cells for cell therapy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Precision Immunoregulation in transplantation: The rise of engineered Treg therapies.Molecular biology reports · 2026Review
- Engineered CD40-biosensor-expressing Treg cells as a cell therapy approach for inflammatory diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Microsystem technologies for accelerating the discovery and translation of immunotherapies.Nature reviews. Drug discovery · 2026Review
- Research progress on chimeric antigen receptor-based immunotherapy against autoimmune diseases.Human vaccines & immunotherapeutics · 2025Review
- Advances in the treatment of systemic lupus erythematosus.Nature reviews. Drug discovery · 2025Review
- Regulatory T Cell-Based Adoptive Cell Therapy in Autoimmunity.International journal of molecular sciences · 2025Review
- Regulatory T cells in cancer anti-PD-(L)1 therapy.Human cell · 2025Review
- Current status of xenotransplantation from an immunobiological standpoint.Clinical transplantation and research · 2025Review
- Harnessing the biology of regulatory T cells to treat disease.Nature reviews. Drug discovery · 2025Review
- Revisiting Tregs in cancer and beyond: immunological control and therapeutic potential.Frontiers in immunology · 2025Review
- Regulatory cell therapy for kidney transplantation and autoimmune kidney diseases.Pediatric nephrology (Berlin, Germany) · 2025Review
- T-regulatory cells for the treatment of autoimmune diseases.Frontiers in immunology · 2025Review
- Inflammation-oriented montmorillonite adjuvant enhanced oral delivery of anti-TNF-α nanobody against inflammatory bowel disease.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Tregs delivered post-myocardial infarction adopt an injury-specific phenotype promoting cardiac repair via macrophages in mice.Nature communications · 2024Article
- Therapeutic induction of antigen-specific immune tolerance.Nature reviews. Immunology · 2024Review
- Genetic engineering of regulatory T cells for treatment of autoimmune disorders including type 1 diabetes.Diabetologia · 2024Review
- Designer cell therapy for tissue regeneration.Inflammation and regeneration · 2024Review
- Selective targeting or reprogramming of intra-tumoral Tregs.Medical oncology (Northwood, London, England) · 2024Review
- Treg-based immunotherapy for antigen-specific immune suppression and stable tolerance induction: a perspective.Immunotherapy advances · 2023Review
- Targeting inflammation to improve regulatory T cell therapy for immunopathologies.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Engineered regulatory T cell (Treg cell) therapy is a promising strategy to treat patients suffering from inflammatory diseases, autoimmunity, and transplant rejection. However, in many cases, disease-related antigens that can be targeted by Treg cells are not available. In this study, we introduce a class of synthetic biosensors, named artificial immune receptors (AIRs), for murine and human Treg cells. AIRs consist of three domains: (a) extracellular binding domain of a tumor necrosis factor (TNF)-receptor superfamily member, (b) intracellular costimulatory signaling domain of CD28, and (c) T cell receptor signaling domain of CD3-ζ chain. These AIR receptors equip Treg cells with an inflammation-sensing machinery and translate this environmental information into a CD3-ζ chain-dependent TCR-activation program. Different AIRs were generated, recognizing the inflammatory ligands of the TNF-receptor superfamily, including LIGHT, TNFα, and TNF-like ligand 1A (TL1A), leading to activation, differentiation, and proliferation of AIR-Treg cells. In a graft-versus-host disease model, Treg cells expressing lymphotoxin β receptor-AIR, which can be activated by the ligand LIGHT, protect significantly better than control Treg cells. Expression and signaling of the corresponding human AIR in human Treg cells prove that this concept can be translated. Engineering Treg cells that target inflammatory ligands leading to TCR signaling and activation might be used as a Treg cell-based therapy approach for a broad range of inflammation-driven diseases.
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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.