IL-4 and IL-13 signaling are two of the key and central drivers of underlying type 2 inflammation in AFRS2-4
ONLY DUPIXENT DIRECTLY INHIBITS IL-4 AND IL-13 SIGNALING TO ADDRESS TWO OF THE KEY AND CENTRAL DRIVERS OF TYPE 2 INFLAMMATION2-4,*
*The mechanism of dupilumab action has not been definitively established.2
DUPIXENT TARGETS TWO OF THE KEY AND CENTRAL DRIVERS OF TYPE 2 INFLAMMATION—IL-4 AND IL-13 SIGNALING2-4,*
DUPIXENT inhibits IL-4 and IL-13 signaling by specifically binding to the IL-4 receptor alpha (IL-4Rα) subunit.2,* Blocking IL-4Rα with DUPIXENT inhibits
IL-4– and IL-13–induced inflammatory responses and lowers total IgE in the blood of patients with AFRS, thereby demonstrating systemic effects of DUPIXENT on these markers of type 2 inflammation in AFRS2,4,9,*:
*The mechanism of dupilumab action has not been definitively established.2
LOCAL
INFLAMMATION
Physiological features3,4,7
- Mucus hypersecretion
- Epithelial barrier dysfunction
Associated clinical features
- Impaired olfactory function1,8
- Tissue remodeling4,10
- Polyp growth and recurrence3,11
- Eosinophilic mucin4
SYSTEMIC
INFLAMMATION3,7
- Elevated IgE levels
AFRS, allergic fungal rhinosinusitis; ILC2, type 2 innate lymphoid cells.