List of works - David Burden

A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1.

scientific article

AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production

scientific article published on 04 July 2016

AP1S3 mutations are associated with pustular psoriasis and impaired Toll-like receptor 3 trafficking

scientific article

Activating CARD14 Mutations Are Associated with Generalized Pustular Psoriasis but Rarely Account for Familial Recurrence in Psoriasis Vulgaris.

scientific article published on 23 July 2015

Clinical and genetic differences between pustular psoriasis subtypes

scientific article published on 21 July 2018

Etanercept or infliximab for psoriasis? An independent randomized clinical trial

scientific article published on March 2017

Filaggrin null alleles are not associated with psoriasis

scientific article published on 5 April 2007

IL36RN mutations define a severe autoinflammatory phenotype of generalized pustular psoriasis

scientific article published on 12 November 2014

Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity.

scientific article

Identification of Rare, Disease-Associated Variants in the Promoter Region of the RNF114 Psoriasis Susceptibility Gene

article

Loss of IL36RN function does not confer susceptibility to psoriasis vulgaris.

scientific article

Meta-analysis confirms the LCE3C_LCE3B deletion as a risk factor for psoriasis in several ethnic groups and finds interaction with HLA-Cw6.

scientific article

Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis.

scientific article

Psoriasis and other complex trait dermatoses: from Loci to functional pathways

scientific article

Rare pathogenic variants in IL36RN underlie a spectrum of psoriasis-associated pustular phenotypes.

scientific article published on 10 January 2013

Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis.

scientific article published on 22 June 2007

List of works by David Burden

A genome-wide association study identifies new psoriasis susceptibility loci and an interaction between HLA-C and ERAP1.

AP1S3 Mutations Cause Skin Autoinflammation by Disrupting Keratinocyte Autophagy and Up-Regulating IL-36 Production

AP1S3 mutations are associated with pustular psoriasis and impaired Toll-like receptor 3 trafficking

Activating CARD14 Mutations Are Associated with Generalized Pustular Psoriasis but Rarely Account for Familial Recurrence in Psoriasis Vulgaris.

Clinical and genetic differences between pustular psoriasis subtypes

Etanercept or infliximab for psoriasis? An independent randomized clinical trial

Filaggrin null alleles are not associated with psoriasis

IL36RN mutations define a severe autoinflammatory phenotype of generalized pustular psoriasis

Identification of 15 new psoriasis susceptibility loci highlights the role of innate immunity.

Identification of Rare, Disease-Associated Variants in the Promoter Region of the RNF114 Psoriasis Susceptibility Gene

Loss of IL36RN function does not confer susceptibility to psoriasis vulgaris.

Meta-analysis confirms the LCE3C_LCE3B deletion as a risk factor for psoriasis in several ethnic groups and finds interaction with HLA-Cw6.

Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis.

Psoriasis and other complex trait dermatoses: from Loci to functional pathways

Rare pathogenic variants in IL36RN underlie a spectrum of psoriasis-associated pustular phenotypes.

Sequence variants in the genes for the interleukin-23 receptor (IL23R) and its ligand (IL12B) confer protection against psoriasis.