ArticleJournal of asthma and allergy2025
TIM-4 Regulates Allergic Airway Inflammation and Mast Cell Activation by Binding to CD300b.
Article in Journal of asthma and allergy, 2025. 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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Abstract
Background: Although T cell immunoglobulin and mucin domain-4 (TIM-4) is involved in immune regulation, the function of TIM-4 in allergic responses is not understood. We investigated the effects of anti-TIM-4 monoclonal antibody (mAb) in a murine model of allergic airway inflammation. Methods: Anti-mouse TIM-4 mAb was administered to various allergic airway inflammatory model mice. A soluble form of TIM-4 (sTIM-4) was detected by newly developed a sandwich Enzyme-Linked Immunosorbent Assay (ELISA) and immunoblotting using anti-mouse or human TIM-4 mAbs. Bone marrow-derived mast cells (BMMCs) were generated from C57BL/6 and CD300b-deficient mice to determine the contribution of sTIM-4 to mast cell activation. The concentrations of serum sTIM-4 in patients with asthma in 124 adult patients were quantified using ELISA. Results: Accumulation of eosinophils and production of T helper type 2 (Th2) cytokines in the lung were significantly reduced in anti-TIM-4-treated mice. High amounts of sTIM-4 through proteolytic cleavage were detected in bronchoalveolar lavage fluid and sera from allergic airway inflammatory mice. sTIM-4 induced proinflammatory cytokine production in mast cells by interacting with CD300b. We also detected human sTIM-4 on TIM-4 transfected cells, which induced interleukin-6 (IL-6) production in a human mast cell line. Moreover, serum sTIM-4 levels were associated with asthma severity in patients with asthma. Conclusion: TIM-4 contributes significantly to the effector phase of allergic airway inflammation. TIM-4 may serve as a therapeutic target and sTIM-4 may have the potential to be used as surrogate marker in asthma.
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