The role of IL-4 in psoriasis

Acute onset of psoriasis in a patient with atopic dermatitis treated with dupilumab

“…Recently, some studies have underlined the negative regulatory action of IL‐4 on the Th1 pathway; it rescues IL‐23 production2 and silences the Th17‐dominated skin inflammation that is predominant in psoriasis. Consequently, it is thought that inhibition of the Th2 pathway through blockage of IL‐4 and IL‐13 signalling could play a role in a shift toward the Th1 inflammatory pathway, which may be responsible for the development of psoriasis in genetically predisposed patients treated with dupilumab 1…”

Occurrence of psoriasiform eruption during dupilumab therapy for adult atopic dermatitis: A case series

“…It has been highlighted that IL-4 downregulates Th1 and Th17 cells and, can modulate dendritic cells thus suppressing IL-23 production. In addition, it can inhibit the secretion of epidermal IL-1b and IL-6 from psoriatic plaques (Hahn & Ghoreschi, 2017;Safa & Paumier, 2019). A case of erythrodermic psoriasis (Tracey et al, 2018) and a case of guttate psoriasis (Gori, Caldarola, Pirro, De Simone, & Peris, 2019) during treatment with dupilumab have been reported.…”

Psoriasis induced by dupilumab therapy

“…The underlying pathophysiological mechanisms that could explain the occurrence of psoriasis following dupilumab treatment remain elusive. Interestingly, in recent experimental studies, it has been shown that IL‐4 can act directly on T cells, dendritic cells and keratinocytes . Furthermore, these studies have shown that IL‐4 is a negative regulator of Th1 and Th17 cells, can modulate the phenotype of dendritic cells resulting in a suppression of IL‐23 production and can inhibit the secretion of IL‐1β and IL‐6 by epidermal cells from psoriatic lesions.…”

“…Interestingly, in recent experimental studies, it has been shown that IL-4 can act directly on T cells, dendritic cells and keratinocytes. 4,5 Furthermore, these studies have shown that IL-4 is a negative regulator of Th1 and Th17 cells, can modulate the phenotype of dendritic cells resulting in a suppression of IL-23 production and can inhibit the secretion of IL-1b and IL-6 by epidermal cells from psoriatic lesions. Accordingly, we hypothesize that blocking the Th2 response with dupilumab by targeting the IL-4/IL-13 signalling pathway could result in a shift toward a Th1/ Th17 phenotype, leading to an inflammatory cytokine cascade and eventually psoriatic skin plaques, as described in this report.…”