Dual inhibition of IL-4 and IL-13 signaling helps1:
REDUCE TYPE 2
INFLAMMATION
REDUCE ITCH
REDUCE HIVES
The mechanism of dupilumab action has not been definitively established.
Type 2 inflammation may contribute to disease chronicity in CSU
Type 2 cytokines, including IL-4 and IL-13, may contribute to
multiple aspects of mast cell activation and degranulation2‑10
Enhance IgE and IgG production
Increase expression of FcεRIa
Enhance neurosensitization to pruritogens
(eg, histamine, other mediators)b
Increase recruitment of type 2 inflammatory cells
(eg, basophils, eosinophils, B cells, and T cells)c
aThis leads to mast cell priming and degranulation. Activated mast cells release IL-4 and IL-13 and contribute to type 2 inflammation in CSU.4
bNeuronal activation can, in turn, induce further immune activation and release inflammatory mediators.11,12
cIL-5 may also play a role in skin homing of eosinophils as well as in their maturation and survival.13
dMast cells can be activated through pathways that are IgE dependent or independent, leading to degranulation and the release of histamine and other immune mediators.6
DUPIXENT is the only dual inhibitor of IL-4 and IL-13 signaling in CSU1,2
DUPIXENT BINDS TO IL-4Rα, INHIBITING IL-4 AND IL-13
INDUCED INFLAMMATORY RESPONSES
The mechanism of dupilumab action has not been definitively established.
aDimerization is when 2 protein subunits combine to form a larger complex. IL-4 signaling through type I receptor requires dimerization of the IL-4Rα with the gamma chain. IL-4 or IL-13 signaling through type II receptor requires dimerization of IL-4Rα with IL-13Rα1.
(TYPE I
RECEPTOR)
SIGNALING
(TYPE II
RECEPTOR)
Assess when your patients might be
ready for DUPIXENT
CSU, chronic spontaneous urticaria; FcεRI, high-affinity IgE receptor.