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Psoriasis News

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A comprehensive genetics study, the result of collaboration between IPC and 3 research institutions, was published in the Nov. 1, 2017 issue of the international research journal Human Molecular Genetics. Entitled “Exome-wide association study reveals novel psoriasis susceptibility locus at TNFSF15 and rare protective alleles in genes contributing to type I IFN signaling,” the study examined common and rare psoriasis-associated gene-centric variation in approximately 40,000 individuals of European descent. The study is part of IPC’s research project, begun in 2013, to complete a genetic “map” of psoriasis that could lead to novel treatment strategies for specific patients and find new therapeutic targets to advance the treatment of the disease. Collaborating on the project with IPC was King’s College London, the University of Michigan, and the University of Kiel in Germany.

The study is the most comprehensive investigation to date of protein-altering variation in psoriasis risk in the European population, said Joelle van der Walt, IPC scientific director. The analysis comprised 4 independent exome array association studies in the United Kingdom, Estonia, Germany, and the United States. The study linked a novel genome-wide association of the TNFSF15 locus with psoriasis risk. This gene encodes a member of the tumor necrosis factor superfamily of cytokines and is expressed in epithelial cells. The study also:

  • established the association of common protein-altering variants at 11 loci previously implicated in psoriasis susceptibility;
  • identified protective variants within the genes IFIH1 and TYK2, both of which play significant roles in type I interferon production and signaling;
  • contributes to the understanding of several mechanisms of psoriasis pathogenesis and suggests that TYK2 may be a potential target for psoriasis drug development.

“This study reveals important factors concerning the genetic basis of psoriasis,” said Professor and IPC Vice President Jonathan Barker, the United Kingdom, who leads IPC’s genetics project. “First it provides evidence of new genetic associations in the TNF-a pathway. It also provides evidence for involvement in virus processing pathways in disease pathogenesis. Finally, it reveals that much of the genetic architecture of psoriasis does not involve protein-coding change and thus is likely to involve other mechanisms such as regulatory elements. “Future work from the international community will involve studies to identify exactly what these regulatory pathways are. Such studies are crucial to the development of bioassays, with which to stratify the disease, predict outcome and potentially aid preventative approaches.”

In addition to Professor Barker, six other IPC councilors were among the researchers who authored the study: Immediate Past President Chris Griffiths, United Kingdom; Kristina Callis Duffin, Gerald Krueger, James Elder, and Johann Gudjonsson, all of the United States; and Ulrich Mrowietz, Germany. The article is available at bit.ly/ PsoGenetics.


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