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Fibrostenosing Crohn’s disease (FSCD) is driven by chronic inflammation, fibroblast activation, extracellular matrix (ECM) deposition and tissue remodeling. Current management includes medical treatment to control inflammation, endoscopic interventions, and surgery to relieve clinically significant strictures. Chimeric antigen receptor (CAR)-based cell therapy represents an emerging research direction that may enable targeted intervention against selected cell populations implicated in fibrogenesis. Unlike approaches focused primarily on inflammatory control, CAR-based strategies can be engineered to recognize selected cellular populations, offering a potential means of directly targeting cells involved in fibrotic remodeling or modulating the local profibrotic microenvironment. By integrating insights from intestinal pathobiology with evidence from other fibrotic settings, we assess candidate cellular targets, therapeutic modalities, and CAR-cell platforms, and consider how these choices should be aligned with lesion accessibility, disease stage, therapeutic objectives, and safety requirements. We further discuss the translational challenges of CAR-based approaches for FSCD.
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Sun et al. (2026) studied this question.
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