Abstract

Sickle Cell Anemia (SCA) is a prevalent inherited blood disorder characterized by abnormal hemoglobin leading to erythrocyte
deformation and consequential vaso-occlusive events. While the primary focus has traditionally centered on the role of red
blood cells in SCA pathophysiology, recent investigations have unveiled the intricate involvement of eosinophils in modulating
disease severity. Eosinophils, classically recognized for their role in parasitic infections and allergic responses, have emerged
as significant contributors to the inflammatory milieu and vascular dysfunction observed in SCA. This paper aims to provide
an extensive understanding of the multifaceted interactions between eosinophils and the pathogenesis of sickle cell anemia,
emphasizing their impact on disease severity. Insights into eosinophil biology, including their cytokine release profile, granule
protein activity, and endothelial interactions, underscore their dual role in both propagating and modulating inflammation in
the context of SCA. The complex interplay between eosinophils and the inflammatory microenvironment in SCA dictates disease
severity, warranting a deeper understanding of these interactions for the development of targeted therapeutic strategies. In
conclusion, this comprehensive review consolidates current knowledge regarding eosinophil involvement in sickle cell anemia
severity, emphasizing the necessity for further investigations into specific eosinophilic mechanisms. A deeper comprehension
of eosinophilic contributions to SCA pathophysiology presents a pathway toward novel therapeutic modalities, ultimately
enhancing the management and porgnosis of individuals afflicted with this challenging hemaotlogic disorder.
Keywords: Sickle Cell Anemia; Eosinophils; Disease Severity; Inflammation; Immune Modulation; Vascular Dysfunction;
Therapeutic Targets