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IL-17 Inhibitor Candidiasis — SCE Rheumatology MCQ

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ModerateSpondyloarthropathyIL-17 Inhibitor CandidiasisSCE Rheumatology

A 42-year-old woman with psoriatic arthritis develops recurrent oral candidiasis after starting secukinumab. Her neutrophil count is normal, and she has no other identified cause of immunodeficiency. Which immunological effect most directly explains this adverse event?

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Correct answer: C — Reduced epithelial antimicrobial-peptide production and neutrophil recruitment at mucosal surfaces

The correct answer is C. IL-17A is central to mucocutaneous defence against Candida. Signalling through epithelial IL-17 receptors induces antimicrobial peptides, including defensins, and chemokines that recruit neutrophils to mucosal surfaces. Secukinumab neutralises IL-17A, selectively weakening this defence and increasing susceptibility to oral, oesophageal and other mucocutaneous candidiasis. Persistent neutropenia is not the principal mechanism: secukinumab-associated neutropenia is uncommon, and the UK SmPC reports no temporal relationship to infection in most affected patients. Interferon-gamma-dependent macrophage activation is more important for intracellular pathogens, terminal complement deficiency predisposes particularly to Neisseria, and defective IgA class switching is not the characteristic effect of IL-17 blockade.

Reference: Mengesha BG, Conti HR. The Role of IL-17 in Protection against Mucosal Candida Infections. Journal of Fungi. 2017;3(4):52. https://pubmed.ncbi.nlm.nih.gov/29371568/