Statistics from Altmetric.com
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.
Since their discovery by Paul Ehrlich in 1879, eosinophils have long been regarded to play a protective role against pathogens, especially during parasite infection.1 Contrary to other granulocytes, eosinophils contain four cationic and acid granule proteins: major basic protein, eosinophil cationic protein (ECP), eosinophil-derived neurotoxin (EDN) and eosinophil peroxidase. In response to external stimuli, these granule proteins are released from eosinophils through piecemeal degranulation, exocytosis or cytolysis, along with proinflammatory chemokines and cytokines.1 When activated, eosinophils induce inflammation that leads to tissue injury and subsequent eosinophil-induced diseases. Of them, asthma is a common airway disease in which eosinophils serve as the key inflammatory cells.
Total eosinophil count (TEC) in the blood is currently the most widely used biomarker for phenotyping asthma and initiating biological agents targeting T2 inflammation. Although higher TEC is related to greater treatment response to corticosteroids and T2-targeting biologics, differences in the clinical course or treatment response among patients with similar levels of blood eosinophils have been noted.2 These findings suggest the heterogeneity in the functional properties of eosinophils in terms of the magnitude of activation and responsiveness to medical treatment, which cannot be assessed by solely counting the number of eosinophils. Therefore, researchers have attempted to identify clinically relevant biomarkers of asthma including eosinophil granule proteins. However, aside from …
Funding This research was supported by the Bio & Medical Technology Development Program of the National Research Foundation (NRF) funded by the Korean government (MSIT) (2019M3E5D3073365).
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.