Inhibition of the Interleukin-36 Pathway for the Treatment of Generalized Pustular Psoriasis

Bachelez, Hervé; Choon, Siew Eng; Marrakchi, Slaheddine; Burden, A. David; Tsai, Tsen‐Fang; Morita, Akimichi; Turki, H.; Hall, David B.; Shear, Michael; Baum, Patrick; Padula, Steven J.; Thoma, Christian

doi:10.1056/nejmc1811317

Cited by 232 publications

(255 citation statements)

References 5 publications

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“…52,53 Of note, inhibition of the IL-36 pathway was recently shown to be efficacious in patients with pustular psoriasis. 54 IL-19 also showed early downregulation by secukinumab in responders, just missing significance (q 5 0.06) in our responder/ nonresponder comparison (not shown). Although IL-19 has mitogenic activity on KCs, 55 we also identified early modulation of the mitogenic epidermal growth factor family members AREG and TGFA in secukinumab responders.…”

Section: Discussionmentioning

confidence: 57%

IL-17A inhibition by secukinumab induces early clinical, histopathologic, and molecular resolution of psoriasis

Krueger

Wharton

Schlitt

et al. 2019

Journal of Allergy and Clinical Immunology

121

116

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and East Hanover, NJ GRAPHICAL ABSTRACT Background: Hyperactivity of the IL-23/IL-17 axis is central to plaque psoriasis pathogenesis. Secukinumab, a fully human mAb that selectively inhibits IL-17A, is approved for treatment of psoriasis, psoriatic arthritis, and ankylosing spondylitis. Secukinumab improves the complete spectrum of psoriasis manifestations, with durable clinical responses beyond 5 years From a the

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Section: Discussionmentioning

confidence: 57%

IL-17A inhibition by secukinumab induces early clinical, histopathologic, and molecular resolution of psoriasis

Krueger

Wharton

Schlitt

et al. 2019

Journal of Allergy and Clinical Immunology

121

116

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“…In addition, Arakawa et al (11) reported that induced IL36RN levels are lower in both GPP patients with and without IL36RN mutations, and proposed "IL36RN insufficiency" in GPP. Consistently, GPP patients can be successfully treated by IL36 signal blockade whether or not IL36RN mutations are present (12). Overall, it seems that the majority of GPP patients have hyperactivation in IL36 signaling.…”

mentioning

confidence: 77%

Autoinflammatory Keratinization Diseases (AiKDs): Expansion of Disorders to Be Included

Akiyama

2020

Front. Immunol.

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“…revealed that the majority of Japanese patients with GPP without PV is caused by IL36RN mutations. Recently, a novel targeted therapy reported that BI 655130, a monoclonal antibody against the IL‐36 receptor, may reduce the severity of GPP, which further verified that the IL‐36 pathway may play a pathogenic role among patients with GPP who have different genetic backgrounds …”

Section: Discussionmentioning

confidence: 85%

“…Recently, a novel targeted therapy reported that BI 655130, a monoclonal antibody against the IL-36 receptor, may reduce the severity of GPP, which further verified that the IL-36 pathway may play a pathogenic role among patients with GPP who have different genetic backgrounds. 11 The present study explored the associations between three polymorphisms (À238A/G, À308A/G, À857C/T) in the TNF gene and the susceptibility to GPP in a Han population from Eastern China for the first time. The results showed that only À238A/G confers GPP risk, with significantly higher A allele, GA and AA genotype frequencies in patients with GPP compared with healthy controls.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor –238A is associated with pediatric‐onset generalized pustular psoriasis in Han patients in Eastern China

Zhao

Sun

et al. 2019

The Journal of Dermatology

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The correlation between polymorphisms at the tumor necrosis factor (TNF) gene and generalized pustular psoriasis (GPP) has rarely been reported. The goal of this study is to investigate whether TNF polymorphisms (−238 A/G, −308 A/G, −857C/T) are associated with susceptibility to GPP in a Han population from Eastern China and to perform subgroup analysis to explore the influence of age onset. Polymorphisms were assessed by polymerase chain reaction amplification and resequencing in 91 GPP patients and 102 healthy controls. The frequencies of the TNF −238A allele and GA+AA genotypes were significantly higher in GPP patients than in those of healthy controls. The subgroup analysis revealed that these significant associations were still present between −238A variants and pediatric‐onset GPP patients who developed GPP at less than 18 years old (PGPP), but not for patients with adult‐onset GPP who developed GPP at 18 years old or more. There were no significant differences in genotype or allele frequencies of TNF −308 A/G and −857C/T polymorphisms between GPP and controls. In conclusion, individuals carrying TNF −238A may be more susceptible to PGPP.

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Inhibition of the Interleukin-36 Pathway for the Treatment of Generalized Pustular Psoriasis

Cited by 232 publications

References 5 publications

IL-17A inhibition by secukinumab induces early clinical, histopathologic, and molecular resolution of psoriasis

IL-17A inhibition by secukinumab induces early clinical, histopathologic, and molecular resolution of psoriasis

Autoinflammatory Keratinization Diseases (AiKDs): Expansion of Disorders to Be Included

Tumor necrosis factor –238A is associated with pediatric‐onset generalized pustular psoriasis in Han patients in Eastern China

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