---
title: "FAP-Targeted CAR Neutrophils from hPSCs Reduce Fibroblast Burden in Cardiac Models"
id: "biorxiv-9-targeting-cardiac-fibrosis-with-chimeric-antigen-receptor-neutrophils-derived"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-9-targeting-cardiac-fibrosis-with-chimeric-antigen-receptor-neutrophils-derived"
content_type: "clinical_feed_article"
specialty: "Cardiology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1?rss=1"
published_at: "2026-10-13T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# FAP-Targeted CAR Neutrophils from hPSCs Reduce Fibroblast Burden in Cardiac Models
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-9-targeting-cardiac-fibrosis-with-chimeric-antigen-receptor-neutrophils-derived
- **Specialty:** [Cardiology](https://medichelpline.com/clinical-feed/cardiology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1?rss=1)
- **Published At:** 2026-10-13T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators engineered neutrophils derived from **human pluripotent stem cells** to express a chimeric antigen receptor (CAR) targeting **fibroblast activation protein (FAP)**. These are referred to in the source as FAP CAR neutrophils. - In vitro co-cultures produced dose-dependent cytotoxicity against activated cardiac fibroblasts in 2D; reactive oxygen species-associated fluorescence increased when CAR neutrophils engaged fibroblasts. - In 3D cardiac organoids, treatment with FAP CAR neutrophils reduced fibroblast-associated fluorescence while cardiomyocyte-associated cardiac troponin T staining remained largely unchanged, indicating selective fibroblast targeting without apparent cardiomyocyte loss. - Phenotypic profiling showed FAP CAR neutrophils had higher inducible nitric oxide synthase (iNOS) and lower Arginase-1 expression compared with unmodified neutrophils, consistent with an N1-like polarization state reported by the authors. - The study team mined public cardiac single-cell and single-nucleus RNA-sequencing datasets to identify temporal patterns of immune signatures and fibroblast activation; those patterns informed suggested treatment timing. - In a murine myocardial infarction model, systemic administration of FAP CAR neutrophils produced higher day-7 left ventricular ejection fraction versus PBS-treated controls in an exploratory comparison reported by the authors. - The report is a preprint and has not undergone peer review; the authors recommended further evaluation and did not provide clinical dosing, safety, or long-term outcome data in the source document. - The source did not report detailed methods for CAR design, neutrophil differentiation protocols, exact dosing regimens in animals, or sample sizes for in vivo experiments; those specifics are absent from the abstract and must be sought in the full manuscript or supplementary material.
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Gyuhyung Jin 1 Purdue University; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gyuhyung%2BJin%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Jin%20G&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGyuhyung%2BJin%2B) * [ORCID record for Gyuhyung Jin](http://orcid.org/0000-0001-9141-1398 "Open in new tab") Shaohai Fang 2 Texas A and M University; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Shaohai%2BFang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Fang%20S&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AShaohai%2BFang%2B) Yun Chang 1 Purdue University; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Yun%2BHuang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Huang%20Y&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AYun%2BHuang%2B) Xiaoping Bao 1 Purdue University; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Xiaoping%2BBao%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bao%20X&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AXiaoping%2BBao%2B) * For correspondence: bao61@purdue.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5864915/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5864915/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5864915/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5864915/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5864915/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Heart failure remains a leading cause of global morbidity and mortality, with cardiac fibrosis contributing to disease progression. Following myocardial injury, activated cardiac fibroblasts orchestrate adverse extracellular matrix (ECM) remodeling, which leads to tissue stiffening and compromised contractility. Despite the clinical importance of cardiac fibrosis, current pharmacological interventions modulate disease progression without directly eliminating activated fibrogenic cells. To target these cells directly, we engineered human pluripotent stem cell (hPSC)-derived neutrophils expressing a chimeric antigen receptor (CAR) directed against fibroblast activation protein (FAP). In vitro, FAP CAR neutrophils exhibited increased reactive oxygen species-associated fluorescence during fibroblast co-culture and dose-dependent cytotoxicity in 2D cultures, while reducing fibroblast-associated fluorescence in 3D cardiac organoids without a significant reduction in cardiomyocyte-associated cardiac troponin T staining. FAP CAR neutrophils also showed increased iNOS and decreased Arginase-1 expression compared with unmodified neutrophils, consistent with a shift toward an N1-associated polarization profile. Analysis of public cardiac single-cell and single-nucleus RNA-sequencing datasets identified temporal patterns of immune-associated expression and fibroblast activation that informed treatment timing. In a murine myocardial infarction (MI) model, mice treated systemically with FAP CAR neutrophils showed higher day 7 left ventricular ejection fraction than PBS-treated mice in an exploratory comparison. Together, these findings support further evaluation of hPSC-derived FAP CAR neutrophils as an immunotherapeutic approach to cardiac fibrosis. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared National Institutes of Health, https://ror.org/01cwqze88, R37CA265926, R35HL166557, R35GM119787 U.S. National Science Foundation, https://ror.org/021nxhr62, CBET-2143064 American Heart Association, https://ror.org/013kjyp64, 23POST1025924, 25POST1373848, 26CDA1609618 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. [Donate to openRxiv ](https://www.zeffy.com/en-US/donation-form/donate-to-make-a-difference-10981) [ Back to top](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1?rss=1#page) [ Previous](https://www.biorxiv.org/content/10.64898/2026.10.11.758319v1 "RTK signaling and epidermis remodeling instruct dendrite regrowth after pruning in the Drosophila PNS") Posted October 13, 2026. [ Download PDF](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/10/13/2026.10.11.758383.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.10.11.758383v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) Targeting Cardiac Fibrosis with Chimeric Antigen Receptor Neutrophils Derived from Human Pluripotent Stem Cells Gyuhyung Jin, Shaohai Fang, Yun Chang, Kunming Shao, Huiyang Li, Yan Tan, Xiaojun Lian, Qing Deng, Yun Huang, Xiaoping Bao bioRxiv 2026.10.11.758383; doi: https://doi.org/10.64898/2026.10.11.758383 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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