Disease drivers: new perspectives on pathogenesis in psoriasis

Date: Friday 24 September 2021
Time: 13.15 – 14.15  PM CET

Objectives:

  1. Explore the latest research on cytokines and cell types that drive disease in psoriasis
  2. Review the disease drivers already targeted by licensed therapies, as well as emerging laboratory, translational and proof-of-concept clinical data from novel pipeline MOA
  3. Expert discussion on how far we have got with understanding the pathogenesis of psoriasis, where we will go next, and what will make a difference to patients



Faculty: 

James Krueger (USA) – Chair

Wolf-Henning Boehncke (Switzerland)



Program

13.15 – 13.16

Welcome and introduction

James Krueger – (USA) Chair

 

13.16 – 13.34

Deconstructing the cytokine cocktail that amplifies inflammation in psoriasis

  • Introduce our current understanding of a cycle of inflammation driven by TNF, the IL-17/23 axis and keratinocyte-produced factors
  • Emerging concepts in the IL-17 family of cytokines
  • IL-23 is elevated in psoriatic lesions and is recognised by IL-23 receptors on T cells to drive release of IL-17A and IL-17F
  • IL-17A and IL-17F are elevated in psoriatic lesions, but can be suppressed with IL-23 inhibition
  • Inhibiting IL-17A or IL-23 suppresses keratinocyte-produced factors
  • IL-17A, IL-17F, IL-23 and IL-19 as potential biomarkers

James Krueger (USA)

13.34 – 13.44

Uncovering the cells that drive disease with cellular profiling

  • New insights from the Human Skin Atlas, which used single-cell RNA sequencing to profile lesional and non-lesional vs healthy skin
  • Profiling tissue-resident memory T cells in psoriatic lesions
  • What open questions remain about dendritic cells and IL-23 production in psoriasis?
  • Identifying distinct populations of IL-17A, IL-17F and IL-17A/F producing cells, including IL-23 independent innate-like lymphocytes
  •  
James Krueger (USA)

13.44 – 13.59

New MOAs in the psoriasis pipeline

  • Review MOAs currently marketed in psoriasis, with a snapshot of MOA data typifying how IL-17Ai, IL-17RAi and IL-23i can dampen disease
  • New evidence on the value of selective inhibition of IL-17F in addition to IL-17A, looking at laboratory, translational and proof-of-concept clinical data from two pipeline therapies
  • Tyk2 inhibition as a less targeted but broader acting approach: translational evidence and proof-of-concept clinical data

Wolf-Henning Boehncke (Switzerland)

13.59 – 14.14

Panel Discussion & Audience Questions

  • How close are we to a definitive picture of pathogenesis in psoriasis?
  • A future role for biomarkers in diagnostics or treatment selection?
  • What will be the next technological or conceptual developments to drive forward research on the pathogenesis of psoriasis?
  • How could new insights on pathogenesis improve the lives of patients?

All, moderated by Chair

14.14 – 14.15

Meeting close

James Krueger – (USA) Chair