ArticleMolecular therapy : the journal of the American Society of Gene Therapy2026
Engineered CD40-biosensor-expressing Treg cells as a cell therapy approach for inflammatory diseases.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Restoring immune tolerance by engineered regulatory T cell (Treg) therapy is a promising strategy to treat patients suffering from autoimmune and inflammatory diseases. However, in many of these conditions, relevant disease-driving antigens are unknown. Therefore, suitable target (auto-)antigens for antigen-specific Treg cell therapy are rarely available. We present a novel artificial immune biosensor for Treg cells that circumvents this limitation by targeting the immune costimulatory protein CD40-ligand (CD40L), transiently expressed by activated T cells. The artificial immune receptor (AIR) comprises a CD40-derived extracellular binding domain, an intracellular costimulatory signaling domain, and a T cell receptor signaling domain of the CD3-ζ-chain. After interaction with its membrane-bound ligand, this synthetic receptor triggers a TCR-like activation program in Treg cells including induction of Treg effector molecules and cell proliferation. In a mouse model of graft-versus-host disease, transfer of CD40-AIR Treg cells significantly improved survival and demonstrated immune control of the alloantigen-reactive T cell compartment. Expression and signaling of the corresponding human CD40-AIR illustrate the potential for translating this concept. Engineering Treg cells with a CD40L-targeting sensor that detects activated T cells presents a promising therapeutic approach for a broad range of T cell-mediated inflammatory diseases.
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