Figure 1.

Working hypothesis of persistent eosinophil inflammation contributing to airway autoimmunity. Priming of eosinophils in the lung tissue leads to activation and degranulation. Based on the triggers or stimuli, eosinophils degranulate (via piecemeal or EETosis) to release more mediators or histone-coated DNA traps. Excessive eosinophilic cytolysis (EETs) becomes a source of self-antigens, tissue damage and damage-associated release of danger-associated molecular patterns (DAMPs) and alarmins. Taken together, this can activate self-reactive lymphocytes and lead to autoimmunity. Autoantibodies (aAbs) cause more EETs and other immune cell activation to release more mediators. The alarmins (TSLP, IL-33) contribute to T2 inflammation and further adds to eosinophilia.