Eosinophil (EOS) (EOS)

Eosinophils are a specialized type of granulocytic white blood cell that serve as key effectors in the innate immune system and primary mediators of Type 2 (Th2) inflammatory responses [1, 6]. They are characterized by large, acidophilic granules containing cytotoxic proteins such as eosinophil peroxidase and major basic protein, which are essential for defense against parasitic helminths but can cause significant tissue damage in pathological states [4, 15]. In conditions such as severe eosinophilic asthma, eosinophilic esophagitis (EoE), and hypereosinophilic syndromes (HES), over-active eosinophils infiltrate target organs, leading to chronic inflammation and tissue remodeling [2, 14, 17]. Therapeutic management of these conditions focuses heavily on the Interleukin-5 (IL-5) signaling pathway, which is critical for eosinophil growth, recruitment, and survival [8, 11]. Biologics such as mepolizumab and benralizumab are used to reduce eosinophil levels in the blood and tissues, effectively decreasing the frequency of asthma exacerbations and improving clinical outcomes [12, 17]. Newer agents also target unique eosinophil surface receptors like Siglec-8 to induce apoptosis or use small molecules like dexpramipexole to inhibit their maturation in the bone marrow [10, 13, 15].

Other names

Eosinophilic granulocyteAcidophilEosEosinophilic leukocyte

Targeted therapies act by: 1) Neutralizing Interleukin-5 (IL-5) to inhibit eosinophil maturation and survival (e.g., mepolizumab, reslizumab) [8, 11]; 2) Binding to the IL-5 receptor alpha (IL-5RA) to block signaling and induce antibody-dependent cellular cytotoxicity (ADCC) for cell depletion (e.g., benralizumab) [4, 12]; 3) Agonizing the inhibitory receptor Siglec-8 to trigger selective eosinophil apoptosis (e.g., lirentelimab) [10, 15]; 4) Inhibiting bone marrow maturation and release of eosinophil progenitors (e.g., dexpramipexole) [13]; and 5) Indirectly reducing recruitment by inhibiting IL-4/IL-13 signaling or inducing glucocorticoid-mediated apoptosis [9, 14].