---
title: "CAR T cell therapy beyond cancer: applications, engineering strategies, and clinical outlook"
id: "pubmed-42575882"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42575882"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42575882/"
doi: "10.1038/s41392-026-02873-4"
published_at: "2026-08-11T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# CAR T cell therapy beyond cancer: applications, engineering strategies, and clinical outlook
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42575882
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42575882/)
- **DOI:** [10.1038/s41392-026-02873-4](https://doi.org/10.1038%2Fs41392-026-02873-4)
- **Published At:** 2026-08-11T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Chimeric antigen receptor (**CAR**) T-cell therapy, whose core strengths are precise antigen recognition and sustained effector activity, is being adapted to eliminate long-lived pathological cells in chronic non-malignant diseases. - Targetable pathological compartments include **viral reservoirs**, autoreactive B and plasma cells, activated fibroblasts, alloimmune clones, and **senescent cells**, all of which can persist despite conventional treatments. - CAR engineering strategies discussed include choice of co-stimulatory domains (CD28, **4-1BB**, OX40) to enhance persistence and function; PD-1–CD28 switch receptors to convert inhibitory signals; and incorporation of dominant-negative **TGF-β** receptors to confer resistance to suppressive microenvironments. - Disease-specific CAR approaches highlighted: CD19- and **BCMA**-directed depletion for autoimmunity; CAR-engineered regulatory T cells (**CAR-Tregs**) for immune regulation; FAP-targeting for fibrosis; B-cell antibody receptor (**BAR**) CARs for hemophilia inhibitors; HLA-specific CAR-Tregs for transplantation tolerance; and uPAR and **NKG2D ligands** targeting for senescence-associated pathologies. - Examples of targeted disease areas include chronic infections (HIV, **EBV**), autoimmune diseases (systemic lupus erythematosus, systemic sclerosis, myositis, multiple sclerosis), fibrotic disease, hemophilia, transplant rejection, and senescence-related disorders. - Early clinical reports and preclinical studies demonstrate feasibility and, in some cases, durable disease modification, though the review emphasizes remaining challenges and the need for further development. - Extending CAR-T beyond oncology reframes programmable cellular immunotherapy as a platform to remove persistent pathological cells, remodel diseased tissue niches, and restore long-term immune homeostasis. - The authors declare no competing interests; the article is a 2026 review in Signal Transduct Target Ther by researchers at Weill Cornell Medicine (Molecular Imaging Innovations Institute).
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY, USA. * 2 Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY, USA. mog4005@med.cornell.edu. # Contributed equally. * PMID: **42575882** * DOI: [ 10.1038/s41392-026-02873-4 ](https://doi.org/10.1038/s41392-026-02873-4) Item in Clipboard Review # CAR T cell therapy beyond cancer: current status, challenges and future prospects Saurabh Upadhyay et al. Signal Transduct Target Ther. 2026. Show details Display options Display options Format Abstract PubMed PMID Signal Transduct Target Ther Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Signal+Transduct+Target+Ther%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Signal+Transduct+Target+Ther%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42575882/) . 2026 Aug 11;11(1):319. doi: 10.1038/s41392-026-02873-4. ### Authors [Saurabh Upadhyay](https://pubmed.ncbi.nlm.nih.gov/?term=Upadhyay+S&cauthor_id=42575882)[#](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-affiliation-1 "Department of Radiology, Molecular Imaging Innovations Institute \(MI3\), Weill Cornell Medicine, New York, NY, USA."), [Sungwoo Cho](https://pubmed.ncbi.nlm.nih.gov/?term=Cho+S&cauthor_id=42575882)[#](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-equal-contrib-explanation "Contributed equally")[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-affiliation-1 "Department of Radiology, Molecular Imaging Innovations Institute \(MI3\), Weill Cornell Medicine, New York, NY, USA."), [Kirti Upmanyu](https://pubmed.ncbi.nlm.nih.gov/?term=Upmanyu+K&cauthor_id=42575882)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-affiliation-1 "Department of Radiology, Molecular Imaging Innovations Institute \(MI3\), Weill Cornell Medicine, New York, NY, USA."), [Moustafa T Gabr](https://pubmed.ncbi.nlm.nih.gov/?term=Gabr+MT&cauthor_id=42575882)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42575882/#short-view-affiliation-2 "Department of Radiology, Molecular Imaging Innovations Institute \(MI3\), Weill Cornell Medicine, New York, NY, USA. mog4005@med.cornell.edu.") ### Affiliations * 1 Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY, USA. * 2 Department of Radiology, Molecular Imaging Innovations Institute (MI3), Weill Cornell Medicine, New York, NY, USA. mog4005@med.cornell.edu. # Contributed equally. * PMID: **42575882** * DOI: [ 10.1038/s41392-026-02873-4 ](https://doi.org/10.1038/s41392-026-02873-4) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Chimeric antigen receptor (CAR) T-cell therapy has revolutionized oncology, and its foundational logic-precise antigen recognition coupled with durable effector activity-extends naturally to chronic non-malignant diseases sustained by long-lived pathological cells. These include viral reservoirs, autoreactive B and plasma cells, activated fibroblasts, alloimmune clones, and senescent cells that remodel tissue niches and evade clearance by conventional therapies. This review highlights how CAR-based strategies can be adapted across diverse disease settings by redirecting engineered immune responses toward disease-sustaining cellular compartments. Co-stimulatory domains such as CD28, 4-1BB, and OX40 enhance persistence and effector function; programmed cell death protein 1 (PD-1)-CD28 switch receptors reverse inhibitory signaling; and cytokine-resistant CARs incorporating dominant-negative transforming growth factor-β (TGF-β) receptors maintain activity within suppressive microenvironments. We discuss these approaches across infections, including human immunodeficiency virus (HIV) and Epstein-Barr virus (EBV); autoimmunity involving CD19- and B-cell maturation antigen (BCMA)-directed depletion strategies and CAR-engineered regulatory T cells (CAR-Tregs); fibrosis targeting fibroblast activation protein (FAP); hemophilia using B-cell antibody receptor (BAR)-CARs against factor VIII and factor IX inhibitors; transplantation employing human leukocyte antigen (HLA)-specific CAR-Tregs; and senescence-associated pathologies targeting urokinase plasminogen activator receptor (uPAR) and natural killer group 2D ligands (NKG2DLs). Early clinical experiences in systemic lupus erythematosus, systemic sclerosis, myositis, and multiple sclerosis, together with preclinical successes in chronic infections and fibrotic disease, demonstrate both feasibility and durable disease modification. By extending CAR-T therapy beyond oncology, these applications position programmable cellular immunotherapy as a broadly adaptable platform for eliminating persistent pathological cells, remodeling diseased tissue environments, and restoring long-term immune homeostasis. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Competing interests: The authors declare no competing interests. ## References 1. 1. Blum, P. & Kayser, S. Chimeric Antigen Receptor (CAR) T-cell therapy in hematologic malignancies: clinical implications and limitations. Cancers 16, 1599 (2024). 2. 1. Peng, L. et al. CAR-T and CAR-NK as cellular cancer immunotherapy for solid tumors. Cell Mol. Immunol. 21, 1089–1108 (2024). - [DOI](https://doi.org/10.1038/s41423-024-01207-0) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/39134804/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/11442786/) 3. 1. Yan, Z. et al. A combination of humanised anti-CD19 and anti-BCMA CAR T cells in patients with relapsed or refractory multiple myeloma: a single-arm, phase 2 trial. Lancet Haematol. 6, e521–e529 (2019). - [PubMed](https://pubmed.ncbi.nlm.nih.gov/31378662/) - [DOI](https://doi.org/10.1016/s2352-3026\(19\)30115-2) 4. 1. Chen, X. et al. Challenges and strategies in clinical applications of CAR-T therapy for autoimmune diseases. J. Hematol. Oncol. 19, 1 (2025). - [DOI](https://doi.org/10.1186/s13045-025-01769-0) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/41316450/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/12763875/) 5. 1. Goetzl, E. J. Expanding therapeutic strategies for chimeric antigen receptor T cells. Am. J. 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