Galectin-10 as a Potential Biomarker for Eosinophilic Diseases
Hiroki Tomizawa,
Yoshiyuki Yamada,
Misaki Arima,
Yui Miyabe,
Mineyo Fukuchi,
Haruka Hikichi,
Rossana C. N. Melo,
Takechiyo Yamada,
Shigeharu Ueki
Affiliations
Hiroki Tomizawa
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Yoshiyuki Yamada
Department of Pediatrics, Tokai University School of Medicine, Isehara 259-1193, Japan
Misaki Arima
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Yui Miyabe
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Mineyo Fukuchi
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Haruka Hikichi
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Rossana C. N. Melo
Laboratory of Cellular Biology, Department of Biology, Institute of Biological Sciences, Federal University of Juiz de Fora, Juiz de Fora 36036-900, MG, Brazil
Takechiyo Yamada
Department of Otorhinolaryngology, Head and Neck Surgery, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Shigeharu Ueki
Clinical Laboratory Medicine, Department of General Internal Medicine, Akita University Graduate School of Medicine, Akita 010-8543, Japan
Galectin-10 is a member of the lectin family and one of the most abundant cytoplasmic proteins in human eosinophils. Except for some myeloid leukemia cells, basophils, and minor T cell populations, galectin-10 is exclusively present in eosinophils in the human body. Galectin-10 forms Charcot–Leyden crystals, which are observed in various eosinophilic diseases. Accumulating studies have indicated that galectin-10 acts as a new biomarker for disease activity, diagnosis, and treatment effectiveness in asthma, eosinophilic esophagitis, rhinitis, sinusitis, atopic dermatitis, and eosinophilic granulomatosis with polyangiitis. The extracellular release of galectin-10 is not mediated through conventional secretory processes (piecemeal degranulation or exocytosis), but rather by extracellular trap cell death (ETosis), which is an active cell death program. Eosinophils undergoing ETosis rapidly disintegrate their plasma membranes to release the majority of galectin-10. Therefore, elevated galectin-10 levels in serum and tissue suggest a high degree of eosinophil ETosis. To date, several studies have shown that galectin-10/Charcot–Leyden crystals are more than just markers for eosinophilic inflammation, but play functional roles in immunity. In this review, we focus on the close relationship between eosinophils and galectin-10, highlighting this protein as a potential new biomarker in eosinophilic diseases.