The role of IL-17 and IL-17 receptor inhibitors in the management
of generalized pustular psoriasis

Plachouri, Kerasia Maria; Chourdakis, Vlassios; Georgiou, Sophia

doi:10.1358/dot.2019.55.9.3020159

Cited by 11 publications

(8 citation statements)

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“…The IL-1 receptor antagonist anakinra and IL-1β inhibitors have been successfully administered in isolated cases [ 158 , 159 , 160 ]. Most recently, the anti-IL17A monoclonal antibodies secukinumab and ixekizumab and the anti-IL-17A receptor monoclonal antibody brodalumab have shown encouraging results [ 130 , 133 , 134 , 135 , 161 ]. Guselkumab, an anti-IL-23p19 agent, demonstrated efficacy in Japanese patients with GPP [ 136 ], whereas a phase III trial with risankizumab, another IL23p19 inhibitor, in Japanese GPP patients has been completed ( Table 4 ).…”

Section: Treatmentmentioning

confidence: 99%

Pustular Psoriasis: From Pathophysiology to Treatment

Genovese

Moltrasio

Cassano³

et al. 2021

Biomedicines

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Pustular psoriasis (PP) is a clinicopathological entity encompassing different variants, i.e., acute generalized PP (GPP), PP of pregnancy (impetigo herpetiformis), annular (and circinate) PP, infantile/juvenile PP, palmoplantar PP/palmoplantar pustulosis, and acrodermatitis continua of Hallopeau (ACH), which have in common an eruption of superficial sterile pustules on an erythematous base. Unlike psoriasis vulgaris, in which a key role is played by the adaptive immune system and interleukin (IL)-17/IL-23 axis, PP seems to be characterized by an intense inflammatory response resulting from innate immunity hyperactivation, with prominent involvement of the IL-36 axis. Some nosological aspects of PP are still controversial and debated. Moreover, owing to the rarity and heterogeneity of PP forms, data on prognosis and therapeutic management are limited. Recent progresses in the identification of genetic mutations and immunological mechanisms have promoted a better understanding of PP pathogenesis and might have important consequences on diagnostic refinement and treatment. In this narrative review, current findings in the pathogenesis, classification, clinical features, and therapeutic management of PP are briefly discussed.

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Section: Treatmentmentioning

confidence: 99%

Pustular Psoriasis: From Pathophysiology to Treatment

Genovese

Moltrasio

Cassano³

et al. 2021

Biomedicines

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“…Considering the upregulation of IL-17 and the pronounced neutrophilic infiltration in the skin of GPP patients, anti-IL-17 treatment appeared to be a very promising option [33]. Three IL-17 inhibitors (secukinumab, ixekizumab, and brodalumab) are currently licensed and approved for the treatment of moderate-to-severe plaque psoriasis [123].…”

Section: Biologic Therapeutics For Gpp In the Light Of Novel Genetic And Immunological Findingsmentioning

confidence: 99%

“…Nonbiological systemic therapy in adult patients typically includes acitretin, cyclosporine A, and methotrexate [25,26]. Only in Japan, several biologics have been approved for the treatment of GPP in patients who had an inadequate response to conventional therapy, including monoclonal antibodies against interleukin (IL)-17 (secukinumab and ixekizumab) or its receptor (brodalumab) and against IL-23 (risankizumab and guselkumab) [27][28][29][30][31][32][33][34]. Since the adaptive immune system plays a critical role in the pathogenesis of plaque psoriasis, agents specifically targeting elements of adaptive immunity are highly efficacious for the treatment of chronic plaque psoriasis [35].…”

Section: Introductionmentioning

confidence: 99%

Generalized Pustular Psoriasis: Divergence of Innate and Adaptive Immunity

Samotij

Szczęch

Reich

2021

IJMS

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Generalized pustular psoriasis (GPP) is a severe, relapsing, immune-mediated disease characterized by the presence of multiple sterile pustules all over the body. The exact pathomechanisms behind GPP remain elusive, although increased interest in the genetic basis and immunological disturbances have provided some revealing insights into the underlying signaling pathways and their mutual interaction. The genetic background of GPP has been thoroughly investigated over the past few years. The conducted studies have identified genetic variants that predispose to pustular forms of psoriasis. The loss-of-function mutation of the interleukin 36 receptor antagonist gene, along with rare gain-of-function mutations in the gene that encodes the keratinocyte signaling molecule (CARD14), are examples of the uncovered abnormalities. Interleukin 36 (IL-36), along with neutrophils, is now considered a central cytokine in GPP pathogenesis, with IL-36 signaling providing a link between innate and adaptive immune responses. More recently, a new concept of inflammation, caused by a predominantly genetically determined abnormal activation of innate immune response and leading to inflammatory keratinization, has arisen. GPP is currently considered a representative of this novel group of skin conditions, called autoinflammatory keratinization diseases. As no therapeutic agents have been approved for GPP to date in the United States and Europe, the novel anti-IL-36R antibodies are particularly promising and may revolutionize management of the disease.

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“…Therefore, it is suggested that some cases of SPD may represent a variant of GPP. The skin lesions of GPP demonstrated an increased expression of Th17 cytokines, such as IL‐17A, that play an important role in the recruitment of neutrophils to the epidermis of patients with psoriasis 4 . Guselkumab neutralizes IL‐23, a key cytokine for Th17 cell differentiation that is mainly produced by dendritic cells.…”

Section: Figurementioning

confidence: 99%