Allergology international : official journal of the Japanese Society of Allergology · 2026
Downregulation of leukocyte immunoglobulin-like receptor B3 is involved in eosinophilic rhinosinusitis.
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Nouchi Yusuke, Takeda Yuji, Suzuki Yusuke, Chiba Makoto, Kawai Yui, Watanabe Chihiro, Abiko Yuko, Saitoh Shinichi, Araki Akemi, Yamaguchi Risako, Yokozawa Junji, Ito Tsukasa, Asao Hironobu
Аннотация
BACKGROUND: Eosinophilic chronic rhinosinusitis (ECRS) is a type 2-mediated inflammatory disease that is often refractory to treatment. The leukocyte immunoglobulin-like receptor (LILR) family plays a critical role in maintaining mast cell and eosinophil homeostasis; however, their involvement in ECRS remains unclear. This study aimed to investigate whether LILR expression in immune cells, particularly eosinophils, is associated with the pathogenesis of ECRS.
METHODS: Peripheral blood and sinus mucosal tissues were collected from patients with ECRS, non-eosinophilic chronic rhinosinusitis (NECRS), non-rhinosinusitis controls, and healthy adults. LILR expression in leukocytes was analyzed by flow cytometry. Serum cytokine levels were measured, and whole blood from healthy adults was stimulated with selected cytokines to assess changes in LILR expression.
RESULTS: Eosinophils selectively expressed LILRB3, an immunosuppressive receptor. While LILRB3 expression on peripheral blood eosinophils did not differ significantly between ECRS and NECRS, tissue eosinophils from patients with ECRS showed markedly lower LILRB3 expression than those from NECRS. Although serum IL-5 levels were significantly elevated in ECRS, IL-5 concentrations did not correlate with LILRB3 expression. Furthermore, the downregulation of LILRB3 was not induced by IL-5 or by other stimulants associated with type 2 inflammation.
CONCLUSIONS: Downregulation of LILRB3 expression in tissue eosinophils is distinctly associated with ECRS, and appears to be regulated by a complex immune microenvironment rather than simply by type 2 cytokines. Further studies are required to clarify the functional consequences and causal role of LILRB3 in ECRS pathogenesis.
METHODS: Peripheral blood and sinus mucosal tissues were collected from patients with ECRS, non-eosinophilic chronic rhinosinusitis (NECRS), non-rhinosinusitis controls, and healthy adults. LILR expression in leukocytes was analyzed by flow cytometry. Serum cytokine levels were measured, and whole blood from healthy adults was stimulated with selected cytokines to assess changes in LILR expression.
RESULTS: Eosinophils selectively expressed LILRB3, an immunosuppressive receptor. While LILRB3 expression on peripheral blood eosinophils did not differ significantly between ECRS and NECRS, tissue eosinophils from patients with ECRS showed markedly lower LILRB3 expression than those from NECRS. Although serum IL-5 levels were significantly elevated in ECRS, IL-5 concentrations did not correlate with LILRB3 expression. Furthermore, the downregulation of LILRB3 was not induced by IL-5 or by other stimulants associated with type 2 inflammation.
CONCLUSIONS: Downregulation of LILRB3 expression in tissue eosinophils is distinctly associated with ECRS, and appears to be regulated by a complex immune microenvironment rather than simply by type 2 cytokines. Further studies are required to clarify the functional consequences and causal role of LILRB3 in ECRS pathogenesis.