Eosinophil recruitment and activation pathways

Eosinophil recruitment and activation pathways are complex biological processes that govern the development, trafficking, and effector functions of eosinophils in various tissues (NIH, 2024; Frontiers in Immunology, 2021). These pathways are primarily orchestrated by Type 2 (Th2) cytokines, with Interleukin-5 (IL-5) serving as the master regulator of eosinophilopoiesis in the bone marrow and survival in the periphery (NIH, 2024; Remedypublications, 2020). Recruitment to inflammatory sites involves a multistep process of tethering, rolling, and firm adhesion mediated by selectins and integrins (e.g., VLA-4), followed by chemotaxis driven by eotaxins (CCL11, CCL24, CCL26) acting on the CCR3 receptor (NIH, 2012; Frontiers in Immunology, 2021). Upon reaching the target tissue, eosinophils undergo activation and degranulation, releasing cytotoxic proteins such as major basic protein (MBP) and eosinophil-derived neurotoxin (EDN), which contribute to tissue damage and airway remodeling in diseases like severe asthma and eosinophilic esophagitis (NIH, 2021; NIH, 2020). Therapeutic intervention focuses on disrupting these pathways using monoclonal antibodies that neutralize IL-5 (mepolizumab, reslizumab), block the IL-5 receptor (benralizumab), or target upstream alarmins like TSLP (tezepelumab) (NIH, 2024; NIH, 2020). While generally safe, these therapies carry theoretical risks related to impaired host defense against parasitic infections and potential hypersensitivity reactions (NIH, 2020; NIH, 2024).

Other names

Eosinophilic inflammation pathwayTh2-mediated eosinophil activationEosinophil trafficking pathwayEosinophilopoiesis and recruitment cascade

Inhibition of eosinophil maturation, recruitment, and activation through the neutralization of cytokines (IL-5, IL-4, IL-13, TSLP) or their receptors, or by inducing eosinophil depletion via antibody-dependent cellular cytotoxicity (ADCC).