A patient with moderate-to-severe plaque psoriasis not responding to methotrexate is started on a biologic. The agent selectively inhibits IL-17A by binding both free IL-17A and IL-17A already bound to its receptor. This mechanism describes:
- A Secukinumab
- B Bimekizumab
- C Ixekizumab ✓
- D Brodalumab
Explanation
Ixekizumab (IgG4 monoclonal antibody) binds IL-17A with high affinity including IL-17A already bound to the IL-17 receptor, blocking signaling. Secukinumab is also an anti-IL-17A antibody but an IgG1 kappa that neutralizes free IL-17A only. Bimekizumab is unique in inhibiting both IL-17A and IL-17F. Brodalumab targets the IL-17 receptor (IL-17RA), thus blocking IL-17A, IL-17F, IL-17A/F heterodimer, and IL-17E/25 — broadest IL-17 pathway blockade. IL-17A is the key effector cytokine in psoriasis pathogenesis, produced by Th17 cells in response to IL-23 produced by dendritic cells and macrophages.
Reference: Neena Khanna Illustrated Synopsis of Dermatology & STD, 6th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.