ReviewMedicinal research reviews2026
Redefining CHI3L1: Therapeutic Opportunities at the Crossroads of Immune Suppression and Disease Progression.
Review in Medicinal research reviews, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors.
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Abstract
Chitinase-3-like-1 (CHI3L1, also known as YKL-40) has been recognized as a biomarker of inflammation and tissue remodeling and has now emerged as a pseudoenzymatic immune checkpoint. Recent structural, immunological, and translational studies redefine it as an active regulator of immune suppression rather than a passive disease marker. Despite lacking catalytic activity, CHI3L1's conserved chitinase fold and glycan-decorated surface acts as a modular scaffold linking cytokine, metabolic, and stress signals to immune suppression and fibrotic remodeling. Through its chitinase-like structure it engages with receptor triad complex, including IL-13Rα2, TMEM219, and Galectin-3, activating signaling pathways such as MAPK, PI3K/AKT, and TGF-β/Smad. Through these interactions, CHI3L1 has been reported to promote fibroblast activation, angiogenesis, and immune suppression, creating environments where immune cells are excluded or silenced. These checkpoint-like effects are not limited to cancer; they also appear in fibrosis, infection, and neuroinflammatory diseases, linking CHI3L1 to a broad spectrum of immune-resistant conditions. This review integrates structural glycobiology, receptor pharmacology, and immunometabolic mechanisms to reveal CHI3L1 as a unifying regulator of stromal-immune crosstalk. It further highlights preclinical and clinical evidence demonstrating that antibody, RNA-based, and small-molecule inhibitors of CHI3L1 restore immune surveillance and limit pathological remodeling. Targeting this pseudoenzymatic checkpoint alongside canonical PD-1 and CTLA-4 blockade represents a promising strategy to overcome immune resistance and normalize pathogenic tissue remodeling across diverse diseases.
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